PART II CHAPTER 4 Sensory Physiologyfac.ksu.edu.sa/sites/default/files/smch4.pdf · 2017-11-22 ·...

Sensory PhysiologyRichard A. Meiss, Ph.D.4

C H A P T E R

4■ THE GENERAL PROBLEM OF SENSATION ■ SPECIFIC SENSORY RECEPTORS

C H A P T E R O U T L I N E

1. Sensory transduction takes place in a series of steps, start-ing with stimuli from the external or internal environmentand ending with neural processing in the central nervoussystem.

2. The structure of sensory organs optimizes their responseto the preferred types of stimuli.

3. A stimulus gives rise to a generator potential, which, inturn, causes action potentials to be produced in the associ-ated sensory nerve.

4. The speeds of adaptation of particular sensory receptorsare related to their biological roles.

5. Specific sensory receptors for a variety of types of tactilestimulation are located in the skin.

6. Somatic pain is associated with the body surface and themusculature; visceral pain is associated with the internalorgans.

7. The sensory function of the eyeball is determined by struc-tures that form and adjust images and by structures thattransform images into neural signals.

8. The retina contains several cell types, each with a specificrole in the process of visual transduction.

9. The rod cells in the retina have a high sensitivity to light butproduce indistinct images without color, while the cones pro-vide sharp color vision with less sensitivity to light.

10. The visual transduction process requires many steps, be-ginning with the absorption of light and ending with anelectrical response.

11. The outer ear receives sound waves and passes them tothe middle ear; they are modified and passed to the innerear, where the process of sound transduction takes place.

12. The transmission of sound through the middle ear greatlyincreases the efficiency of its detection, while its protectivemechanisms guard the inner ear from damage caused byextremely loud sounds. Disturbances in this transmissionprocess can lead to hearing impairments.

13. Sound vibrations enter the cochlea through the oval win-dow and travel along the basilar membrane, where theirenergy is transformed into neural signals in the organ of Corti.

14. Displacements of the basilar membrane cause deformationof the hair cells, the ultimate transducers of sound. Differ-ent sites along the basilar membrane are sensitive to dif-ferent frequencies.

15. The vestibular apparatus senses the position of the headand its movements by detecting small deflections of itssensory structures.

16. Taste is mediated by sensory epithelial cells in the tastebuds. There are five fundamental taste sensations: sweet,sour, salty, bitter, and umami.

17. Smell is detected by nerve cells in the olfactory mucosa.Thousands of different odors can be detected and distin-guished.

K E Y C O N C E P T S

PART II Neurophysiology

63

64 PART II NEUROPHYSIOLOGY

The survival of any organism, human included, de-pends on having adequate information about the ex-

ternal environment, where food is to be found and wherehazards abound. Equally important for maintaining thefunction of a complex organism is information about thestate of numerous internal bodily processes and functions.Events in our external and internal worlds must first betranslated into signals that our nervous systems canprocess. Despite the wide range of types of information tobe sensed and acted on, a small set of common principlesunderlie all sensory processes.

This chapter discusses the functions of the organs thatpermit us to gather this information, the sensory receptors.The discussion emphasizes somatic sensations, those deal-ing with the external aspect of the body, and does notspecifically treat visceral sensations, those that come frominternal organs.

THE GENERAL PROBLEM OF SENSATION

While the human body contains a very large number of dif-ferent sensory receptors, they have many functional fea-tures in common. Some basic themes are shared by almostall receptors, and the wide variety of specialized functionsis a result of structural and physiological adaptations thatadapt a particular receptor for its role in the overall econ-omy of an organism.

Sensory Receptors Translate Energy From the

Environment Into Biologically Useful Information

The process of sensation essentially involves sampling se-lected small amounts of energy from the environmentand using it to control the generation of action potentialsor nerve impulses (see Fig. 4.1). This process is the func-tion of sensory receptors, biological structures that canbe as simple as a free nerve ending or as complicated asthe human eye or ear. The pattern of sensory action po-tentials, along with the specific nature of the sensory re-ceptor and its nerve pathways in the brain, provide an in-ternal representation of a specific component of theexternal world. The process of sensation is a portion ofthe more complex process of perception, in which sen-sory information is integrated with previously learned in-formation and other sensory inputs, enabling us to makejudgments about the quality, intensity, and relevance ofwhat is being sensed.

The Nature of Environmental Stimuli. A factor in theenvironment that produces an effective response in a sen-sory receptor is called a stimulus. Stimuli involve ex-changes of energy between the environment and the re-ceptors. Typical stimuli include electromagneticquantities, such as radiant heat or light; mechanical quan-tities, such as pressure, sound waves, and other vibrations;and chemical qualities, such as acidity and molecular shapeand size. Common to all these types of stimuli is the prop-erty of intensity, a measure of the energy content (or con-centration, in the case of chemical stimuli) available to in-teract with the sensory receptor. It is not surprising,

therefore, that a fundamental property of receptors is theirability to respond to different intensities of stimulationwith an appropriate output. Also related to receptor func-tion is the concept of sensory modality. This term refersto the kind of sensation, which may range from the rela-tively general modalities of taste, smell, touch, sight, andhearing (the traditional five senses), to more complex sen-sations, such as slipperiness or wetness. Many sensorymodalities are a combination of simpler sensations; thesensation of wetness is composed of sensations of pressureand temperature. (Try placing your hand in a plastic bagand immersing it in cold water. Although the skin will re-main dry, the perception will be one of wetness.)

It is often difficult to communicate a precise definitionof a sensory modality because of the subjective perceptionor affect that accompanies it. This property has to do withthe psychological feeling attached to the stimulus. Somestimuli may give rise to an impression of discomfort orpleasure apart from the primary sensation of, for example,cold or touch. Previous experience and learning play a rolein determining the affect of a sensory perception.

Some sensory receptors are classified by the nature of thesignals they sense. For example, photoreceptors sense lightand serve a visual function. Chemoreceptors detect chemi-cal signals and serve the senses of taste and smell, as well asdetecting the presence of specific substances in the body.Mechanoreceptors sense physical deformation, serve thesenses of touch and hearing, and can detect the amount ofstress in a tendon or muscle; and thermal receptors detectheat (or its relative lack). Other sensory receptors are classi-fied by their “vantage point” in the body. Among these, ex-teroceptors detect stimuli from outside the body; entero-ceptors detect internal stimuli; proprioceptors (receptors of“one’s own”) provide information about the positions ofjoints and about muscle activity and the orientation of thebody in space. Nociceptors (pain receptors) detect noxiousagents, both internally and externally.

Accessorystructures

Centralnervoussystem

Train ofnerve impulses

over specificnerve pathway

Environmentalstimulus

(light, sound,temperature, etc.)

Perception oftype and

intensity ofenvironmental

stimulus

Feedbackcontrol

Sensoryreceptor

A basic model for the translation of an en-

vironmental stimulus into a perception.

While the details vary with each type of sensory modality, theoverall process is similar.

FIGURE 4.1

The Specificity of Sensory Receptors. Most sensory re-ceptors respond preferentially to a single kind of environ-mental stimulus. The usual stimulus for the eye is light; thatfor the ear is sound. This specificity is due to several featuresthat match a receptor to its preferred stimulus. In manycases, accessory structures, such as the lens of the eye orthe structures of the outer and middle ears, enhance the spe-cific sensitivity of the receptor or exclude unwanted stimuli.Often these accessory structures are a control system thatadjusts their sensitivity according to the information beingreceived (Fig. 4.1). The usual and appropriate stimulus for areceptor is called its adequate stimulus. For the adequatestimulus, the receptor has the lowest threshold, the loweststimulus intensity that can be reliably detected. A thresholdis often difficult to measure because it can vary over timeand with the presence of interfering stimuli or the action ofaccessory structures. Although most receptors will respondto stimuli other than the adequate stimulus, the thresholdfor inappropriate stimuli is much higher. For example, gen-tly pressing the outer corner of the eye will produce a visualsensation caused by pressure, not light; extremes of temper-ature may be perceived as pain. Almost all receptors can bestimulated electrically to produce sensations that mimic theone usually associated with that receptor.

The central nervous pathway over which sensory infor-mation travels is also important in determining the natureof the perception; information arriving by way of the opticnerve, for example, is always perceived as light and never assound. This is known as the concept of the labeled line.

The Process of Sensory Transduction Changes

Stimuli Into Biological Information

This section focuses on the actual function of the sensoryreceptor in translating environmental energy into actionpotentials, the fundamental units of information in thenervous system. A device that performs such a translation iscalled a transducer; sensory receptors are biological trans-ducers. The sequence of electrical events in the sensorytransduction process is shown in Figure 4.2.

The Generator Potential. The sensory receptor in thisexample is a mechanoreceptor. Deformation or deflectionof the tip of the receptor gives rise to a series of action po-tentials in the sensory nerve fiber leading to the centralnervous system (CNS). The stimulus (1) is applied at thetip of the receptor, and the deflection (2) is held constant(dotted lines). This deformation of the receptor causes a

CHAPTER 4 Sensory Physiology 65

4

3

2

1

�20

�40

�60

mV

Stimulator

Recordingelectrodes

Impulseinitiation region

Deflectionof receptor

Sensory neuron

0 1

Seconds

To centralnervous system

2 3

Stimulus

Action potentials

Generator potential

Localexcitatorycurrents

The relation between an applied stimulus and the production of sensory nerve action

potentials. (See text for details.)FIGURE 4.2


portion of its cell membrane (shaded region [3]) to be-come more permeable to positive ions (especially sodium).The increased permeability of the membrane leads to a lo-calized depolarization, called the generator potential. Atthe depolarized region, sodium ions enter the cell downtheir electrochemical gradient, causing a current to flow inthe extracellular fluid. Because current is flowing into thecell at one place, it must flow out of the cell in anotherplace. It does this at a region of the receptor membrane (4)called the impulse initiation region (or coding region) be-cause here the flowing current causes the cell membrane toproduce action potentials at a frequency related to thestrength of the current caused by the stimulus. These cur-rents, called local excitatory currents, provide the link be-tween the formation of the generator potential and the ex-citation of the nerve fiber membrane.

In complex sensory organs that contain a great many in-dividual receptors, the generator potential may be called areceptor potential, and it may arise from several sourceswithin the organ. Often the receptor potential is given aspecial name related to the function of the receptor; for ex-ample, in the ear it is called the cochlear microphonic,while an electroretinogram may be recorded from the eye.Note that in the eye the change in receptor membrane po-tential associated with the stimulus of light is a hyperpolar-ization, not a depolarization.

The production of the generator potential is of criticalimportance in the transduction process because it is thestep in which information related to stimulus intensity andduration is transduced. The strength (intensity) of the stim-ulus applied (in Fig. 4.2, the amount of deflection) deter-mines the size of the generator potential depolarization.Varying the intensity of the stimulation will correspond-ingly vary the generator potential, although the changeswill not usually be directly proportional to the intensity.This is called a graded response, in contrast to the all-or-

none response of an action potential, and it causes a similargradation of the strength of the local excitatory currents.These, in turn, determine the amount of depolarizationproduced in the impulse initiation region (4) of the recep-tor, and events in this region constitute the next importantlink in the process.

The Initiation of Nerve Impulses

Figure 4.3 shows a variety of possible events in the impulseinitiation region. The threshold (colored line) is a criticallevel of depolarization; membrane potential changes be-low this level are caused by the local excitatory currentsand vary in proportion to them, while the membrane ac-tivity above the threshold level consists of locally pro-duced action potentials. The lower trace shows a series ofdifferent stimuli applied to the receptor, and the uppertrace shows the resulting electrical events in the impulseinitiation region.

No stimulus is given at A, and the membrane voltage is atthe resting potential. At B, a small stimulus is applied, pro-ducing a generator potential too small to bring the impulseinitiation region membrane to threshold, and no action po-tential activity results. (Such a stimulus would not be sensedat all.) A brief stimulus of greater intensity is given at C; theresulting generator potential displacement is of sufficientamplitude to trigger a single action potential. As in all ex-citable and all-or-none nerve membranes, the action poten-tial is immediately followed by repolarization, often to alevel that transiently hyperpolarizes the membrane poten-tial because of temporarily high potassium conductance.Since the brief stimulus has been removed by this time, nofurther action potentials are produced. A longer stimulus ofthe same intensity (D) produces repetitive action potentialsbecause as the membrane repolarizes from the action po-tential, local excitatory currents are still flowing. They bring

Threshold

Sensory nerve activity with different stimu-

lus intensities and durations. A, With nostimulus, the membrane is at rest. B, A subthreshold stimulus pro-duces a generator potential too small to cause membrane excita-

FIGURE 4.3 tion. C, A brief, but intense, stimulus can cause a single action po-tential. D, Maintaining this stimulus leads to a train of action po-tentials. E, Increasing the stimulus intensity leads to an increase inthe action potential firing rate.

the repolarized membrane to threshold at a rate propor-tional to their strength. During this time interval, the fastsodium channels of the membrane are being reset, and an-other action potential is triggered as soon as the membranepotential reaches threshold. As long as the stimulus is main-tained, this process will repeat itself at a rate determined bythe stimulus intensity. If the intensity of the stimulus is in-creased (E), the local excitatory currents will be strongerand threshold will be reached more rapidly. This will resultin a reduction of the time between each action potentialand, as a consequence, a higher action potential frequency.This change in action potential frequency is critical in com-municating the intensity of the stimulus to the CNS.

Adaptation. The discussion thus far has depicted thegenerator potential as though it does not change when aconstant stimulus is applied. Although this is approximatelycorrect for a few receptors, most will show some degree ofadaptation. In an adapting receptor, the generator poten-tial and, consequently, the action potential frequency willdecline even though the stimulus is maintained. Part A ofFigure 4.4 shows the output from a receptor in which thereis no adaptation. As long as the stimulus is maintained,there is a steady rate of action potential firing. Part B showsslow adaptation; as the generator potential declines, the in-terval between the action potentials increases correspond-ingly. Part C demonstrates rapid adaptation; the action po-tential frequency falls rapidly and then maintains a constantslow rate that does not show further adaptation. Responsesin which there is little or no adaptation are called tonic,whereas those in which significant adaptation occurs arecalled phasic. In some cases, tonic receptors may be calledintensity receptors, and phasic receptors called velocityreceptors. Many receptors—muscle spindles, for exam-ple—show a combination of responses; on application of astimulus, a rapidly adapting phasic response is followed bya steady tonic response. Both of these responses may begraded by the intensity of the stimulus. As a receptoradapts, the sensory input to the CNS is reduced, and thesensation is perceived as less intense.

The phenomenon of adaptation is important in prevent-ing “sensory overload,” and it allows less important or un-changing environmental stimuli to be partially ignored.When a change occurs, however, the phasic response willoccur again, and the sensory input will become temporarilymore noticeable. Rapidly adapting receptors are also im-portant in sensory systems that must sense the rate ofchange of a stimulus, especially when its intensity can varyover a range that would overload a tonic receptor.

Receptor adaptation can occur at several places in thetransduction process. In some cases, the receptor’s sensitiv-ity is changed by the action of accessory structures, as inthe constriction of the pupil of the eye in the presence ofbright light. This is an example of feedback-controlledadaptation; in the sensory cells of the eye, light-controlledchanges in the amounts of the visual pigments also canchange the basic sensitivity of the receptors and produceadaptation. As mentioned above, adaptation of the genera-tor potential can produce adaptation of the overall sensoryresponse. Finally, the phenomenon of accommodation inthe impulse initiation region of the sensory nerve fiber can

slow the rate of action potential production even thoughthe generator potential may show no change. Accommo-dation refers to a gradual increase in threshold caused byprolonged nerve depolarization, resulting from the inacti-vation of sodium channels.

The Perception of Sensory Information Involves

Encoding and Decoding

After the acquisition of sensory stimuli, the process of per-ception involves the subsequent encoding and transmission ofthe sensory signal to the central nervous system. Further pro-cessing or decoding yields biologically useful information.

Encoding and Transmission of Sensory Information.Environmental stimuli that have been partially processedby a sensory receptor must be conveyed to the CNS in such


AAction

potentials

Stimulus

Generatorpotential

Noadaptation

Slowadaptation

Rapidadaptation

Seconds

0 1 2 3

BAction

potentials

Generatorpotential

CAction

potentials

Generatorpotential

Adaptation. Adaptation in a sensory receptoris often related to a decline in the generator po-

tential with time. A, The generator potential is maintained with-out decline, and the action potential frequency remains constant.B, A slow decline in the generator potential is associated withslow adaptation. C, In a rapidly adapting receptor, the generatorpotential declines rapidly.

FIGURE 4.4


a way that the complete range of the intensity of the stim-ulus is preserved.

Compression. The first step in the encoding process iscompression. Even when the receptor sensitivity is modi-fied by accessory structures and adaptation, the range of in-put intensities is quite large, as shown in Figure 4.5. At theleft is a 100-fold range in the intensity of a stimulus. At theright is an intensity scale that results from events in the sen-sory receptor. In most receptors, the magnitude of the gen-erator potential is not exactly proportional to the stimulusintensity; it increases less and less as the stimulus intensityincreases. The frequency of the action potentials producedin the impulse initiation region is also not proportional tothe strength of the local excitatory currents; there is an up-per limit to the number of action potentials per second be-cause of the refractory period of the nerve membrane.These factors are responsible for the process of compres-sion; changes in the intensity of a small stimulus cause agreater change in action potential frequency than the samechange would cause if the stimulus intensity were high. Asa result, the 100-fold variation in the stimulus is compressedinto a threefold range after the receptor has processed thestimulus. Some information is necessarily lost in thisprocess, but integrative processes in the CNS can restorethe information or compensate for its absence. Physiologi-cal evidence for compression is based on the observed non-linear (logarithmic or power function) relation between theactual intensity of a stimulus and its perceived intensity.

Information Transfer. The next step is to transfer thesensory information from the receptor to the CNS. The en-coding processes in the receptors have already providedthe basis for this transfer by producing a series of action po-tentials related to the stimulus intensity. A special processis necessary for the transfer because of the nature of theconduction of action potentials. As an action potential trav-els along a nerve fiber, it is sequentially recreated at a se-

quence of locations along the nerve. Its duration and am-plitude do not change. The only information that can beconveyed by a single action potential is its presence or ab-sence. However, relationships between and among actionpotentials can convey large amounts of information, andthis is the system found in the sensory transmission process.This biological process can be explained by analogy to aphysical system such as that used for transmission of signalsin communications systems.

Figure 4.6 outlines a hypothetical frequency-modulated(FM) encoding, transmission, and reception system. An in-put signal provided by some physical quantity (1) is con-tinuously measured and converted into an electrical signal(2), analogous to the generator potential, whose amplitudeis proportional to the input signal. This signal then controlsthe frequency of a pulse generator (3), as in the impulse ini-tiation region of a sensory nerve fiber. Like action poten-tials, these pulses are of a constant height and duration, andthe amplitude information of the original input signal isnow contained in the intervals between the pulses. The re-sulting signals may be sent along a transmission line (anal-ogous to a nerve pathway) to some distant point, wherethey produce an electrical voltage (4) proportional to thefrequency of the arriving pulses. This voltage is a replica ofthe input voltage (2) and is not affected by changes in theamplitude of the pulses as they travel along the transmis-sion line. Further processing can produce a graphic record(5) of the input data. In a biological system, these latterfunctions are accompanied by processing and interpreta-tion in the CNS.

The Interpretation of Sensory Information. The interpre-tation of encoded and transmitted information into a per-ception requires several other factors. For instance, the in-terpretation of sensory input by the CNS depends on theneural pathway it takes to the brain. All information arrivingon the optic nerves is interpreted as light, even though thesignal may have arisen as a result of pressure applied to theeyeball. The localization of a cutaneous sensation to a par-ticular part of the body also depends on the particular path-way it takes to the CNS. Often a sensation (usually pain)arising in a visceral structure (e.g., heart, gallbladder) is per-ceived as coming from a portion of the body surface, be-cause developmentally related nerve fibers come from theseanatomically different regions and converge on the samespinal neurons. Such a sensation is called referred pain.

SPECIFIC SENSORY RECEPTORS

The remainder of this chapter surveys specific sensory re-ceptors, concentrating on the special senses. These tradi-tionally include cutaneous sensation (touch, temperature,etc.), sight, hearing, taste, and smell.

Cutaneous Sensation Provides Information From

the Body Surface

The skin is richly supplied with sensory receptors servingthe modalities of touch (light and deep pressure), tempera-ture (warm and cold), and pain, as well as the more compli-

Compression in sensory process. By a vari-ety of means, a wide range of input intensities

is coded into a much narrower range of responses that can be rep-resented by variations in action potential frequency.

FIGURE 4.5

cated composite modalities of itch, tickle, wet, and so on.By using special probes that deliver highly localized stimuliof pressure, vibration, heat, or cold, the distribution of cu-taneous receptors over the skin can be mapped. In general,areas of skin used in tasks requiring a high degree of spatiallocalization (e.g., fingertips, lips) have a high density ofspecific receptors, and these areas are correspondingly wellrepresented in the somatosensory areas of the cerebral cor-tex (see Chapter 7).

Tactile Receptor. Several receptor types serve the sensa-tions of touch in the skin (Fig. 4.7). In regions of hairlessskin (e.g., the palm of the hand) are found Merkel’s disks,Meissner’s corpuscles, and pacinian corpuscles. Merkel’sdisks are intensity receptors (located in the lowest layers ofthe epidermis) that show slow adaptation and respond tosteady pressure. Meissner’s corpuscles adapt more rapidlyto the same stimuli and serve as velocity receptors. ThePacinian corpuscles are very rapidly adapting (accelera-tion) receptors. They are most sensitive to fast-changingstimuli, such as vibration. In regions of hairy skin, small

hairs serve as accessory structures for hair-follicle recep-tors, mechanoreceptors that adapt more slowly. Ruffiniendings (located in the dermis) are also slowly adapting re-ceptors. Merkel’s disks in areas of hairy skin are groupedinto tactile disks. Pacinian corpuscles also sense vibrationsin hairy skin. Nonmyelinated nerve endings, also usuallyfound in hairy skin, appear to have a limited tactile functionand may sense pain.

Temperature Sensation. From a physical standpoint,warm and cold represent values along a temperature contin-uum and do not differ fundamentally except in the amountof molecular motion present. However, the familiar subjec-tive differentiation of the temperature sense into “warm” and“cold” reflects the underlying physiology of the two popula-tions of receptors responsible for thermal sensation.

Temperature receptors (thermoreceptors) appear to benaked nerve endings supplied by either thin myelinatedfibers (cold receptors) or nonmyelinated fibers (warm re-ceptors) with low conduction velocity. Cold receptorsform a population with a broad response peak at about


Environmentalstimulus

(e.g., temperature)

Analog signal(varying voltage)

Transmitted FMsignal

(varying frequency)

Demodulatedsignal

(varying voltage)

Replica of theenvironmental

stimulus

Physicalsystem

Transducer

Modulator

Transmissionline

Demodulator

Scaling andreadout

Biologicalsystem

Sensory receptor/Generator potential

Impulse initiationregion

Nerve pathway

CNS processing

Further CNSprocessing andinterpretation

Time

Deg

rees

Deg

rees

Pul

ses/

sec

Vol

tsV

olts

1

2

3

4

5

The transmission of sensory information.

Because signals of varying amplitude cannot betransmitted along a nerve fiber, specific intensity information istransformed into a corresponding action potential frequency, andCNS processes decode the nerve activity into biologically useful

FIGURE 4.6 information. The steps in the process are shown at the left, withthe parts of a physical system that perform them (FM, frequencymodulation). At the right are the analogous biological steps in-volved in the same process.


30�C; the warm receptor population has its peak at about43�C (Fig. 4.8). Both sets of receptors share some commonfeatures:• They are sensitive only to thermal stimulation.• They have both a phasic response that is rapidly adapt-

ing and responds only to temperature changes (in a fash-ion roughly proportional to the rate of change) and atonic (intensity) response that depends on the localtemperature.The density of temperature receptors differs at different

places on the body surface. They are present in much lowernumbers than cutaneous mechanoreceptors, and there aremany more cold receptors than warm receptors.

The perception of temperature stimuli is closely relatedto the properties of the receptors. The phasic componentof the response is apparent in our adaptation to sudden im-mersion in, for example, a warm bath. The sensation ofwarmth, apparent at first, soon fades away, and a less in-tense impression of the steady temperature may remain.Moving to somewhat cooler water produces an immediatesensation of cold that soon fades away. Over an intermedi-ate temperature range (the “comfort zone”), there is no ap-preciable temperature sensation. This range is approxi-mately 30 to 36�C for a small area of skin; the range isnarrower when the whole body is exposed. Outside this

range, steady temperature sensation depends on the ambi-ent (skin) temperature. At skin temperatures lower than17�C, cold pain is sensed, but this sensation arises frompain receptors, not cold receptors. At very high skin tem-peratures (above 45�C), there is a sensation of paradoxicalcold, caused by activation of a part of the cold receptorpopulation.

Temperature perception is subject to considerable pro-cessing by higher centers. While the perceived sensationsreflect the activity of specific receptors, the phasic compo-nent of temperature perception may take many minutes tobe completed, whereas the adaptation of the receptors iscomplete within seconds.

Pain. The familiar sensation of pain is not limited to cu-taneous sensation; pain coming from stimulation of thebody surface is called superficial pain, while that arisingfrom within muscles, joints, bones, and connective tissue iscalled deep pain. These two categories comprise somaticpain. Visceral pain arises from internal organs and is oftendue to strong contractions of visceral muscle or its forcibledeformation.

Pain is sensed by a population of specific receptorscalled nociceptors. In the skin, these are the free endings ofthin myelinated and nonmyelinated fibers with characteris-tically low conduction velocities. They typically have ahigh threshold for mechanical, chemical, or thermal stimuli(or a combination) of intensity sufficient to cause tissue de-struction. The skin has many more points at which pain canbe elicited than it has mechanically or thermally sensitivesites. Because of the high threshold of pain receptors (com-pared with that of other cutaneous receptors), we are usu-ally unaware of their existence.

Superficial pain may often have two components: an im-mediate, sharp, and highly localizable initial pain; and, af-ter a latency of about 1 second, a longer-lasting and morediffuse delayed pain. These two submodalities appear to bemediated by different nerve fiber endings. In addition to

Hornylayer

Subcutaneoustissue

Epidermis

Dermis

Hairless skin Hairy skin

Hair-folliclereceptor

Merkel’sdisks

Ruffiniending

Paciniancorpuscle

Meissner’scorpuscle

Tactiledisks

Tactile receptors in the skin. (See text fordetails.)

FIGURE 4.7

Warm fibers

Responses of cold and warm receptors in

the skin. The skin temperature was held at dif-ferent values while nerve impulses were recorded from representa-tive fibers leading from each receptor type. (Modified from Ken-shalo. In: Zotterman Y. Sensory Functions of Skin in Primates.Oxford: Pergamon, 1976.)

FIGURE 4.8

their normally high thresholds, both cutaneous and deeppain receptors show little adaptation, a fact that is unpleas-ant but biologically necessary. Deep and visceral pain ap-pear to be sensed by similar nerve endings, which may alsobe stimulated by local metabolic conditions, such as is-chemia (lack of adequate blood flow, as may occur duringthe heart pain of angina pectoris).

The free nerve endings mediating pain sensation areanatomically distinct from other free nerve endings in-volved in the normal sensation of mechanical and thermalstimuli. The functional differences are not microscopicallyevident and are likely to relate to specific elements in themolecular structure of the receptor cell membrane.

The Eye Is a Sensor for Vision

The eye is an exceedingly complex sensory organ, involv-ing both sensory elements and elaborate accessory struc-tures that process information both before and after it is de-tected by the light-sensitive cells. A satisfactoryunderstanding of vision involves a knowledge of some ofthe basic physics of light and its manipulation, in additionto the biological aspects of its detection.

The Properties of Light and Lenses. The adequate stim-ulus for human visual receptors is light, which may be de-fined as electromagnetic radiation between the wave-lengths of 770 nm (red) and 380 nm (violet). The familiarcolors of the spectrum all lie between these limits. A widerange of intensities, from a single photon to the direct lightof the sun, exists in nature.

As with all such radiation, light rays travel in a straightline in a given medium. Light rays are refracted or bent asthey pass between media (e.g., glass, air) that have differentrefractive indices. The amount of bending is determinedby the angle at which the ray strikes the surface; if the an-gle is 90�, there is no bending, while successively moreoblique rays are bent more sharply. A simple prism (Fig.4.9A) can, therefore, cause a light ray to deviate from itspath and travel in a new direction. An appropriately chosenpair of prisms can turn parallel rays to a common point (Fig.4.9B). A convex lens may be thought of as a series of suchprisms with increasingly more bending power (Fig. 4.9C,D), and such a lens, called a converging lens or positivelens, will bring an infinite number of parallel rays to a com-mon point, called the focal point. A converging lens canform a real image. The distance from the lens to this pointis its focal length (FL), which may be expressed in meters.A convex lens with less curvature has a longer focal length(Fig. 4.9E). Often the diopter (D), which is the inverse ofthe focal length (1/FL), is used to describe the power of alens. For example, a lens with a focal length of 0.5 meter hasa power of 2 D. An advantage of this system is that dioptricpowers are additive; two convex lenses of 25 D each willfunction as a single lens with a power of 50 D when placednext to each other (Fig. 4.9F).

A concave lens causes parallel rays to diverge (Fig.4.9G). Its focal length (and its power in diopters) is nega-tive, and it cannot form a real image. A concave lens placedbefore a positive lens lengthens the focal length (Fig. 4.9H)of the lens system; the diopters of the two lenses are added

algebraically. External lenses (eyeglasses or contact lenses)are used to compensate for optical defects in the eye.

The Structure of the Eye. The human eyeball is a roughlyspherical organ, consisting of several layers and structures(Fig. 4.10). The outermost of these consists of a tough,white, connective tissue layer, the sclera, and a transparentlayer, the cornea. Six extraocular muscles that control thedirection of the eyeball insert on the sclera. The next layeris the vascular coat; its rear portion, the choroid, is pig-mented and highly vascular, supplying blood to the outerportions of the retina. The front portion contains the iris, acircular smooth muscle structure that forms the pupil, theneurally controlled aperture through which light is admit-ted to the interior of the eye. The iris also gives the eye itscharacteristic color.

The transparent lens is located just behind the iris and isheld in place by a radial arrangement of zonule fibers, sus-pensory ligaments that attach it to the ciliary body, whichcontains smooth muscle fibers that regulate the curvature ofthe lens and, hence, its focal length. The lens is composedof many thin, interlocking layers of fibrous protein and ishighly elastic.

Between the cornea and the iris/lens is the anteriorchamber, a space filled with a thin clear liquid called theaqueous humor, similar in composition to cerebrospinal


How lenses control the refraction of light.

A, A prism bends the path of parallel rays oflight. B, The amount of bending varies with the prism shape. C,A series of prisms can bring parallel rays to a point. D, The limit-ing case of this arrangement is a convex (converging) lens. E,Such a lens with less curvature has a longer focal length. F, Plac-ing two such lenses together produces a shorter focal length. G,A concave (negative) lens causes rays to diverge. H, A negativelens can effectively increase the focal length of a positive lens.

FIGURE 4.9


fluid. This liquid is continuously secreted by the epitheliumof the ciliary processes, located behind the iris. As the fluidaccumulates, it is drained through the canal of Schlemminto the venous circulation. (Drainage of aqueous humor iscritical. If too much pressure builds up in the anterior cham-ber, the internal structures are compressed and glaucoma, acondition that can cause blindness, results.) The posteriorchamber lies behind the iris; along with the anterior cham-ber, it makes up the anterior cavity. The vitreous humor(or vitreous body), a clear gelatinous substance, fills thelarge cavity between the rear of the lens and the front sur-face of the retina. This substance is exchanged much moreslowly than the aqueous humor.

The innermost layer of the eyeball is the retina, wherethe optical image is formed. This tissue contains the pho-toreceptor cells, called rods and cones, and a complex mul-tilayered network of nerve fibers and cells that function inthe early stages of image processing. The rear of the retinais supplied with blood from the choroid, while the front issupplied by the central artery and vein that enter the eye-ball with the optic nerve, the fiber bundle that connectsthe retina with structures in the brain. The vascular supplyto the front of the retina, which ramifies and spreads overthe retinal surface, is visible through the lens and affords adirect view of the microcirculation; this window is usefulfor diagnostic purposes, even for conditions not directly re-lated to ocular function.

At the optical center of the retina, where the imagefalls when one is looking straight ahead (i.e., along the vi-sual axis), is the macula lutea, an area of about 1 mm2 spe-cialized for very sharp color vision. At the center of themacula is the fovea centralis, a depressed region about 0.4mm in diameter, the fixation point of direct vision.Slightly off to the nasal side of the retina is the optic disc,where the optic nerve leaves the retina. There are no pho-

toreceptor cells here, resulting in a blind spot in the fieldof vision. However, because the two eyes are mirror im-ages of each other, information from the overlapping vi-sual field of one eye “fills in” the missing part of the imagefrom the other eye.

The Optics of the Eye. The image that falls on the retinais real and inverted, as in a camera. Neural processing re-stores the upright appearance of the field of view. The im-age itself can be modified by optical adjustments made bythe lens and the iris. Most of the refractive power (about 43D) is provided by the curvature of the cornea, with the lensproviding an additional 13 to 26 D, depending on the focaldistance. The muscle of the ciliary body has primarily aparasympathetic innervation, although some sympatheticinnervation is present. When it is fully relaxed, the lens isat its flattest and the eye is focused at infinity (actually, atanything more than 6 meters away) (Fig. 4.11A). When theciliary muscle is fully contracted, the lens is at its mostcurved and the eye is focused at its nearest point of distinctvision (Fig. 4.11B). This adjustment of the eye for close vi-sion is called accommodation. The near point of vision forthe eye of a young adult is about 10 cm. With age, the lensloses its elasticity and the near point of vision moves fartheraway, becoming approximately 80 cm at age 60. This con-dition is called presbyopia; supplemental refractive power,

Vitreous humor

FoveaOptic disc(blind spot)

Lens

Visual axisCorneaAnterior chamber

IrisPosteriorchamber

Pupil

Canal of Schlemm

Ciliary body

Zonulefibers

Ciliaryprocess

Retina

Choroid

ScleraOptic nerve

The major parts of the human eye. This is aview from above, showing the relative positions

of its optical and structural parts.

FIGURE 4.10

The eye as an optical device. During fixationthe center of the image falls on the fovea. A,

With the lens flattened, parallel rays from a distant object arebrought to a sharp focus. B, Lens curvature increases with accom-modation, and rays from a nearby object are focused.

FIGURE 4.11

in the form of external lenses (reading glasses), is requiredfor distinct near vision.

Errors of refraction are common (Fig. 4.12). They can becorrected with external lenses (eyeglasses or contactlenses). Farsightedness or hyperopia is caused by an eyeballthat is physically too short to focus on distant objects. Thenatural accommodation mechanism may compensate fordistance vision, but the near point will still be too far away;the use of a positive (converging) lens corrects this error. Ifthe eyeball is too long, nearsightedness or myopia results.In effect, the converging power of the eye is too great; closevision is clear, but the eye cannot focus on distant objects.A negative (diverging) lens corrects this defect. If the cur-vature of the cornea is not symmetric, astigmatism results.Objects with different orientations in the field of view willhave different focal positions. Vertical lines may appearsharp, while horizontal structures are blurred. This condi-tion is corrected with the use of a cylindrical lens, whichhas different radii of curvature at the proper orientationsalong its surfaces. Normal vision (i.e., the absence of anyrefractive errors) is termed emmetropia (literally, “eye inproper measure”).

Normally the lens is completely transparent to visiblelight. Especially in older adults, there may be a progressiveincrease in its opacity, to the extent that vision is obscured.This condition, called a cataract, is treated by surgical re-moval of the defective lens. An artificial lens may be im-planted in its place, or eyeglasses may be used to replacethe refractive power of the lens.

The iris, which has both sympathetic and parasympa-thetic innervation, controls the diameter of the pupil. It iscapable of a 30-fold change in area and in the amount oflight admitted to the eye. This change is under complex re-flex control, and bright light entering just one eye willcause the appropriate constriction response in both eyes.As with a camera, when the pupil is constricted, less lightenters, but the image is focused more sharply because themore poorly focused peripheral rays are cut off.

Eye Movements. The extraocular muscles move theeyes. These six muscles, which originate on the bone of theorbit (the eye socket) and insert on the sclera, are arrangedin three sets of antagonistic pairs. They are under visuallycompensated feedback control and produce several typesof movement:• Continuous activation of a small number of motor units

produces a small tremor at a rate of 30 to 80 cycles persecond. This movement and a slow drift cause the imageto be in constant motion on the retina, a necessary con-dition for proper visual function.

• Larger movements include rapid flicks, called saccades,which suddenly change the orientation of the eyeball,and large, slow movements, used in following movingobjects.Organized movements of the eyes include:

• Fixation, the training of the eyes on a stationary object• Tracking movements, used to follow the course of a

moving target


The use of external lenses to correct refrac-

tive errors. The external optical correctionsFIGURE 4.12 change the effective focal length of the natural optical compo-

nents.


• Convergence adjustments, in which both eyes turn in-ward to fix on near objects

• Nystagmus, a series of slow and saccadic movements(part of a vestibular reflex) that serves to keep the retinalimage steady during rotation of the head.Because the eyes are separated by some distance, each

receives a slightly different image of the same object. Thisproperty, binocular vision, along with information aboutthe different positions of the two eyes, allows stereoscopicvision and its associated depth perception, abilities that arelargely lost in the case of blindness in one eye. Many ab-normalities of eye movement are types of strabismus(“squinting”), in which the two eyes do not work togetherproperly. Other defects include diplopia (double vision),when the convergence mechanisms are impaired, and am-blyopia, when one eye assumes improper dominance overthe other. Failure to correct this latter condition can lead toloss of visual function in the subordinate eye.

The Retina and Its Photoreceptors. The retina is a multi-layered structure containing the photoreceptor cells and acomplex web of several types of nerve cells (Fig. 4.13).There are 10 layers in the retina, but this discussion em-ploys a simpler four-layer scheme: pigment epithelium,photoreceptor layer, neural network layer, and ganglioncell layer. These four layers are discussed in order, begin-ning with the deepest layer (pigment epithelium) and mov-ing toward the layer nearest to the inner surface of the eye(ganglion cell layer). Note that this is the direction inwhich visual signal processing takes place, but it is oppositeto the path taken by the light entering the retina.

Pigment Epithelium. The pigment epithelium(Fig. 4.13B) consists of cells with high melanin content.This opaque material, which also extends between portionsof individual rods and cones, prevents the scattering of straylight, thereby greatly sharpening the resolving power of theretina. Its presence ensures that a tiny spot of light (or a tinyportion of an image) will excite only those receptors onwhich it falls directly. People with albinism lack this pig-ment and have blurred vision that cannot be corrected ef-fectively with external lenses. The pigment epithelial cellsalso phagocytose bits of cell membrane that are constantlyshed from the outer segments of the photoreceptors.

Photoreceptor Layer. In the photoreceptor layer (Fig.4.13C), the rods and cones are packed tightly side-by-side,with a density of many thousands per square millimeter, de-pending on the region of the retina. Each eye containsabout 125 million rods and 5.5 million cones. Because ofthe eye’s mode of embryologic development, the photore-ceptor cells occupy a deep layer of the retina, and lightmust pass through several overlying layers to reach them.The photoreceptors are divided into two classes. The conesare responsible for photopic (daytime) vision, which is incolor (chromatic), and the rods are responsible for scotopic(nighttime) vision, which is not in color. Their functionsare basically similar, although they have important struc-tural and biochemical differences.

Cones have an outer segment that tapers to a point (Fig.4.14). Three different photopigments are associated withcone cells. The pigments differ in the wavelength of light

that optimally excites them. The peak spectral sensitivityfor the red-sensitive pigment is 560 nm; for the green-sen-sitive pigment, it is about 530 nm; and for the blue-sensi-tive pigment, it is about 420 nm. The corresponding pho-toreceptors are called red, green, and blue cones,respectively. At wavelengths away from the optimum, thepigments still absorb light but with reduced sensitivity. Be-cause of the interplay between light intensity and wave-length, a retina with only one class of cones would not beable to detect colors unambiguously. The presence of twoof the three pigments in each cone removes this uncer-tainty. Colorblind individuals, who have a genetic lack ofone or more of the pigments or lack an associated trans-duction mechanism, cannot distinguish between the af-

A

B

D

E

C

Organization of the human retina. A,Choroid. B, Pigment epithelium. C, Photore-

ceptor layer. D, Neural network layer. E, Ganglion cell layer. r,rod; c, cone; h, horizontal cell; b, bipolar cell; a, amacrine cell; g,ganglion cell. (See text for details.) (Modified from Dowling JE,Boycott BB. Organization of the primate retina: Electron mi-croscopy. Proc Roy Soc Lond 1966:166:80–111.

FIGURE 4.13

fected colors. Loss of a single color system producesdichromatic vision and lack of two of the systems causesmonochromatic vision. If all three are lacking, vision ismonochromatic and depends only on the rods.

A rod cell is long, slender, and cylindrical and is largerthan a cone cell (Fig. 4.14). Its outer segment contains nu-merous photoreceptor disks composed of cellular mem-brane in which the molecules of the photopigmentrhodopsin are embedded. The lamellae near the tip are reg-ularly shed and replaced with new membrane synthesizedat the opposite end of the outer segment. The inner seg-ment, connected to the outer segment by a modified cil-ium, contains the cell nucleus, many mitochondria thatprovide energy for the phototransduction process, andother cell organelles. At the base of the cell is a synapticbody that makes contact with one or more bipolar nervecells and liberates a transmitter substance in response tochanging light levels.

The visual pigments of the photoreceptor cells convertlight to a nerve signal. This process is best understood as itoccurs in rod cells. In the dark, the pigment rhodopsin (orvisual purple) consists of a light-trapping chromophorecalled scotopsin that is chemically conjugated with 11-cis-retinal, the aldehyde form of vitamin A1. When struck bylight, rhodopsin undergoes a series of rapid chemical tran-sitions, with the final intermediate form metarhodopsin IIproviding the critical link between this reaction series andthe electrical response. The end-products of the light-in-duced transformation are the original scotopsin and an all-trans form of retinal, now dissociated from each other. Un-der conditions of both light and dark, the all-trans form of

retinal is isomerized back to the 11-cis form, and therhodopsin is reconstituted. All of these reactions take placein the highly folded membranes comprising the outer seg-ment of the rod cell.

The biochemical process of visual signal transduction isshown in Figure 4.15. The coupling of the light-induced re-actions and the electrical response involves the activationof transducin, a G protein; the associated exchange of GTPfor GDP activates a phosphodiesterase. This, in turn, cat-alyzes the breakdown of cyclic GMP (cGMP) to 5’-GMP.When cellular cGMP levels are high (as in the dark), mem-brane sodium channels are kept open, and the cell is rela-tively depolarized. Under these conditions, there is a tonicrelease of neurotransmitter from the synaptic body of therod cell. A decrease in the level of cGMP as a result of light-induced reactions causes the cell to close its sodium chan-nels and hyperpolarize, thus, reducing the release of neuro-transmitter; this change is the signal that is furtherprocessed by the nerve cells of the retina to form the finalresponse in the optic nerve. An active sodium pump main-


Outer segment(with disk-shaped

lamellae)

Inner segment(with cell organelles)

Nucleus

Synaptic body

Cone Rod

Photoreceptors of the human retina. Coneand rod receptors are compared. (Modified

from Davson H, ed. The Eye: Visual Function in Man. 2nd Ed.New York: Academic, 1976.)

FIGURE 4.14

PassiveNa+

influx(dark

current)

Steady transmitterrelease is reducedby light-dependenthyperpolarization

Light

Na+

K+

Na+

Na+

Disk membrane

Rod cellmembrane

5' GMPcGMP

GDP

GTP

GC

++

+PDE

TR

Dark currentNa+ entry

ActiveNa+

efflux

Lowercytoplasmic

cGMP closesNa+ channels,

hyperpolarizes cell

RH*

The biochemical process of visual signal

transduction. Left: An active Na�/K� pumpmaintains the ionic balance of a rod cell, while Na� enters pas-sively through channels in the plasma membrane, causing a main-tained depolarization and a dark current under conditions of nolight. Right: The amplifying cascade of reactions (which takeplace in the disk membrane of a photoreceptor) allows a singleactivated rhodopsin molecule to control the hydrolysis of500,000 cGMP molecules. (See text for details of the reaction se-quence.) In the presence of light, the reactions lead to a depletionof cGMP, resulting in the closing of cell membrane Na� channelsand the production of a hyperpolarizing generator potential. Therelease of neurotransmitter decreases during stimulation by light.RH*, activated rhodopsin; TR, transducin; GC, guanylyl cyclase;PDE, phosphodiesterase.

FIGURE 4.15


tains the cellular concentration at proper levels. A large am-plification of the light response takes place during the cou-pling steps; one activated rhodopsin molecule will activateapproximately 500 transducins, each of which activates thehydrolysis of several thousand cGMP molecules. Underproper conditions, a rod cell can respond to a single pho-ton striking the outer segment. The processes in cone cellsare similar, although there are three different opsins (withdifferent spectral sensitivities) and the specific transductionmechanism is also different. The overall sensitivity of thetransduction process is also lower.

In the light, much rhodopsin is in its unconjugated form,and the sensitivity of the rod cell is relatively low. Duringthe process of dark adaptation, which takes about 40 min-utes to complete, the stores of rhodopsin are gradually builtup, with a consequent increase in sensitivity (by as much as25,000 times). Cone cells adapt more quickly than rods, buttheir final sensitivity is much lower. The reverse process,light adaptation, takes about 5 minutes.

Neural Network Layer. Bipolar cells, horizontal cells,and amacrine cells comprise the neural network layer.These cells together are responsible for considerable initialprocessing of visual information. Because the distances be-tween neurons here are so small, most cellular communica-tion involves the electrotonic spread of cell potentials,rather than propagated action potentials. Light stimulationof the photoreceptors produces hyperpolarization that istransmitted to the bipolar cells. Some of these cells respondwith a depolarization that is excitatory to the ganglioncells, whereas other cells respond with a hyperpolarizationthat is inhibitory. The horizontal cells also receive inputfrom rod and cone cells but spread information laterally,causing inhibition of the bipolar cells on which theysynapse. Another important aspect of retinal processing islateral inhibition. A strongly stimulated receptor cell can,via lateral inhibitory pathways, inhibit the response ofneighboring cells that are less well-illuminated. This hasthe effect of increasing the apparent contrast at the edge ofan image. Amacrine cells also send information laterally butsynapse on ganglion cells.

Ganglion Cell Layer. In the ganglion cell layer (Fig.4.13E) the results of retinal processing are finally integratedby the ganglion cells, whose axons form the optic nerve.These cells are tonically active, sending action potentialsinto the optic nerve at an average rate of five per second,even when unstimulated. Input from other cells convergingon the ganglion cells modifies this rate up or down.

Many kinds of information regarding color, brightness,contrast, and so on are passed along the optic nerve. Theoutput of individual photoreceptor cells is convergent onthe ganglion cells. In keeping with their role in visual acu-ity, relatively few cone cells converge on a ganglion cell,especially in the fovea, where the ratio is nearly 1:1. Rodcells, however, are highly convergent, with as many as 300rods converging on a single ganglion cell. While this mech-anism reduces the sharpness of an image, it allows for agreat increase in light sensitivity.

Central Projections of the Retina. The optic nerves, eachcarrying about 1 million fibers from each retina, enter the

rear of the orbit and pass to the underside of the brain tothe optic chiasma, where about half the fibers from eacheye “cross over” to the other side. Fibers from the temporalside of the retina do not cross the midline, but travel in theoptic tract on the same side of the brain. Fibers originatingfrom the nasal side of the retina cross the optic chiasma andtravel in the optic tract to the opposite side of the brain.Hence, information from right and left visual fields is trans-mitted to opposite sides of the brain. The divided outputgoes through the optic tract to the paired lateral geniculatebodies (part of the thalamus) and then via the geniculocal-carine tract (or optic radiation) to the visual cortex in theoccipital lobe of the brain (Fig. 4.16). Specific portions ofeach retina are mapped to specific areas of the cortex; thefoveal and macular regions have the greatest representa-tion, while the peripheral areas have the least. Mechanismsin the visual cortex detect and integrate visual information,such as shape, contrast, line, and intensity, into a coherentvisual perception.

Information from the optic nerves is also sent to thesuprachiasmatic nucleus of the hypothalamus, where itparticipates in the regulation of circadian rhythms; the pre-tectal nuclei, concerned with the control of visual fixationand pupillary reflexes; and the superior colliculus, which

Optic nerve

Lateralgeniculate

body

Visualcortex

Geniculo-calcarine

tract

Optictract

Opticchiasma

The CNS pathway for visual information.

Fibers from the right visual field will stimulatethe left half of each retina, and nerve impulses will be transmittedto the left hemisphere.

FIGURE 4.16

coordinates simultaneous bilateral eye movements, such astracking and convergence.

The Ear Is Sensor for Hearing and Equilibrium

The human ear has a degree of complexity probably as greatas that of the eye. Understanding our sense of hearing re-quires familiarity with the physics of sound and its interac-tions with the biological structures involved in hearing.

The Nature of Sound. Sound waves are mechanical dis-turbances that travel through an elastic medium (usually airor water). A sound wave is produced by a mechanically vi-brating structure that alternately compresses and rarefiesthe air (or water) in contact with it. For example, as a loud-speaker cone moves forward, air molecules in its path areforced closer together; this is called compression or con-densation. As the cone moves back, the space between thedisturbed molecules is increased; this is known as rarefac-tion. The compression (or rarefaction) of air molecules inone region causes a similar compression in adjacent re-gions. Continuation of this process causes the disturbance(the sound wave) to spread away from the source.

The speed at which the sound wave travels is deter-mined by the elasticity of the air (the tendency of the mol-ecules to spring back to their original positions). Assumingthe sound source is moving back and forth at a constant rateof alternation (i.e., at a constant frequency), a propagatedcompression wave will pass a given point once for every cy-cle of the source. Because the propagation speed is constantin a given medium, the compression waves are closer to-gether at higher frequencies; that is, more of them pass thegiven point every second.

The distance between the compression peaks is calledthe wavelength of the sound, and it is inversely related tothe frequency. A tone of 1,000 cycles per second, travel-ing through the air, has a wavelength of approximately34 cm, while a tone of 2,000 cycles per second has awavelength of 17 cm. Both waves, however, travel at thesame speed through the air. Because the elastic forces inwater are greater than those in air, the speed of sound inwater is about 4 times as great, and the wavelength is cor-respondingly increased. Since the wavelength dependson the elasticity of the medium (which varies accordingto temperature and pressure), it is more convenient toidentify sound waves by their frequency. Sound fre-quency is usually expressed in units of Hertz (Hz or cy-cles per second).

Another fundamental characteristic of a sound wave isits intensity or amplitude. This may be thought of as therelative amount of compression or rarefaction present asthe wave is produced and propagated; it is related to theamount of energy contained in the wave. Usually the in-tensity is expressed in terms of sound pressure, the pres-sure the compressions and rarefactions exert on a surface ofknown area (expressed in dynes per square centimeter). Be-cause the human ear is sensitive to sounds over a million-fold range of sound pressure levels, it is convenient to ex-press the intensity of sound as the logarithm of a ratioreferenced to the absolute threshold of hearing for a toneof 1,000 Hz. This reference level has a value of 0.0002

dyne/cm2, and the scale for the measurements is the deci-bel (dB) scale. In the expression

dB � 20 log (P/Pref), (1)

the sound pressure (P) is referred to the absolute referencepressure (Pref). For a sound that is 10 times greater than thereference, the expression becomes

dB � 20 log (0.002 / 0.0002) � 20. (2)

Thus, any two sounds having a tenfold difference in in-tensity have a decibel difference of 20; a 100-fold differ-ence would mean a 40 dB difference and a 1,000-fold dif-ference would be 60 dB. Usually the reference value isassumed to be constant and standard, and it is not expressedwhen measurements are reported.

Table 4.1 lists the sound pressure levels and the decibellevels for some common sounds. The total range of 140 dBshown in the table expresses a relative range of 10 million-fold. Adaptation and compression processes in the humanauditory system allow encoding of most of this wide rangeinto biologically useful information.

Sinusoidal sound waves contain all of their energy atone frequency and are perceived as pure tones. Complexsound waves, such as those in speech or music, consist ofthe addition of several simpler waveforms of different fre-quencies and amplitudes. The human ear is capable of hear-ing sounds over the range of 20 to 16,000 Hz, although theupper limit decreases with age. Auditory sensitivity varieswith the frequency of the sound; we hear sounds most read-ily in the range of 1,000 to 4,000 Hz and at a sound pres-sure level of around 60 dB. Not surprisingly, this is the fre-quency and intensity range of human vocalization. Theear’s sensitivity is also affected by masking: In the presenceof background sounds or noise, the auditory threshold for agiven tone rises. This may be due to refractoriness inducedby the masking sound, which would reduce the number ofavailable receptor cells.

The Outer Ear. An overall view of the human ear is shownin Figure 4.17. The pinna, the visible portion of the outerear, is not critical to hearing in humans, although it does


TABLE 4.1 The Relative Pressures of Some

Common Sounds

SoundPressure Pressure Relative

(dynes/cm2) Level (dB) Sound Source Pressure

0.0002 0 Absolute threshold 10.002 � 20 Faint whisper 100.02 � 40 Quiet office 1000.2 � 60 Conversation 1,002 � 80 City bus 10,000

20 �100 Subway train 100,000200 �120 Loud thunder 1,000,000

2,000 �140 Pain and damage 10,000,000

Modified from Gulick WL, Gescheider GA, Frisina RD. Hearing:Physiological Acoustics, Neural Coding, and Psychoacoustics. NewYork: Oxford University Press, 1989, Table 2.2, p. 51.


slightly emphasize frequencies in the range of 1,500 to7,000 Hz and aids in the localization of sources of sound.The external auditory canal extends inward through thetemporal bone. Wax-secreting glands line the canal, and itsinner end is sealed by the tympanic membrane or eardrum,a thin, oval, slightly conical, flexible membrane that is an-chored around its edges to a ring of bone. An incomingpressure wave traveling down the external auditory canalcauses the eardrum to vibrate back and forth in step withthe compressions and rarefactions of the sound wave. Thisis the first mechanical step in the transduction of sound.The overall acoustic effect of the outer ear structures is toproduce an amplification of 10 to 15 dB in the frequencyrange broadly centered around 3,000 Hz.

The Middle Ear. The next portion of the auditory sys-tem is an air-filled cavity (volume about 2 mL) in the mas-toid region of the temporal bone. The middle ear is con-nected to the pharynx by the eustachian tube. The tubeopens briefly during swallowing, allowing equalization ofthe pressures on either side of the eardrum. During rapidexternal pressure changes (such as in an elevator ride orduring takeoff or descent in an airplane), the unequalforces displace the eardrum; such physical deformationmay cause discomfort or pain and, by restricting the mo-tion of the tympanic membrane, may impair hearing.Blockages of the eustachian tube or fluid accumulation inthe middle ear (as a result of an infection) can also lead todifficulties with hearing.

Bridging the gap between the tympanic membrane andthe inner ear is a chain of three very small bones, the ossi-cles (Fig. 4.18). The malleus (hammer) is attached to theeardrum in such a way that the back-and-forth movementof the eardrum causes a rocking movement of the malleus.The incus (anvil) connects the head of the malleus to thethird bone, the stapes (stirrup). This last bone, through its

oval footplate, connects to the oval window of the innerear and is anchored there by an annular ligament.

Four separate suspensory ligaments hold the ossicles inposition in the middle ear cavity. The superior and lateral lig-aments lie roughly in the plane of the ossicular chain and an-chor the head and shaft of the malleus. The anterior ligamentattaches the head of the malleus to the anterior wall of themiddle ear cavity, and the posterior ligament runs from thehead of the incus to the posterior wall of the cavity. The sus-pensory ligaments allow the ossicles sufficient freedom tofunction as a lever system to transmit the vibrations of thetympanic membrane to the oval window. This mechanism isespecially important because, although the eardrum is sus-pended in air, the oval window seals off a fluid-filled cham-ber. Transmission of sound from air to liquid is inefficient; ifsound waves were to strike the oval window directly, 99.9%of the energy would be reflected away and lost.

Two mechanisms work to compensate for this loss. Al-though it varies with frequency, the ossicular chain has alever ratio of about 1.3:1, producing a slight gain in force.In addition, the relatively large area of the tympanic mem-brane is coupled to the smaller area of the oval window (ap-proximately a 17:1 ratio). These conditions result in a pres-sure gain of around 25 dB, largely compensating for thepotential loss. Although the efficiency depends on the fre-quency, approximately 60% of the sound energy thatstrikes the eardrum is transmitted to the oval window.

Outer ear

Pinna

Externalauditory

canal

Cochlearnerve

Middleear

Inner ear

Incus

PosteriorSuperior

Lateral

Semicircularcanals

Vestibular nerve

Facial nerve

Vestibule

The overall structure of the human ear. Thestructures of the middle and inner ear are en-

cased in the temporal bone of the skull.

FIGURE 4.17

Innerear

Middleear

Eustachian tube

Outerear

EardrumTensor

tympanimuscle

Lateralligament

Temporal bone

Approximateaxis ofrotation

Superiorligament

Stapediusmuscle

Basilarmembrane

Oval window

Stapes

IncusMalleus

Roundwindow

Scalitympani

Scala vestibuli

A model of the middle ear. Vibrations fromthe eardrum are transmitted by the lever system

formed by the ossicular chain to the oval window of the scalavestibuli. The anterior and posterior ligaments, part of the sus-pensory system for the ossicles, are not shown. The combinationof the four suspensory ligaments produces a virtual pivot point(marked by a cross); its position varies with the frequency and in-tensity of the sound. The stapedius and tensor tympani musclesmodify the lever function of the ossicular chain.

FIGURE 4.18

Sound transmission through the middle ear is also af-fected by the action of two small muscles that attach to theossicular chain and help hold the bones in position andmodify their function (see Fig. 4.18). The tensor tympanimuscle inserts on the malleus (near the center of theeardrum), passes diagonally through the middle ear cavity,and enters the tensor canal, in which it is anchored. Con-traction of this muscle limits the vibration amplitude of theeardrum and makes sound transmission less efficient. Thestapedius muscle attaches to the stapes near its connectionto the incus and runs posteriorly to the mastoid bone. Itscontraction changes the axis of oscillation of the ossicularchain and causes dissipation of excess movement before itreaches the oval window. These muscles are activated by areflex (simultaneously in both ears) in response to moder-ate and loud sounds; they act to reduce the transmission ofsound to the inner ear and, thus, to protect its delicatestructures. Because this acoustic reflex requires up to 150msec to operate (depending on the loudness of the stimu-lus), it cannot provide protection from sharp or suddenbursts of sound.

The process of sound transmission can bypass the ossic-ular chain entirely. If a vibrating object, such as a tuningfork, is placed against a bone of the skull (typically the mas-toid), the vibrations are transmitted mechanically to thefluid of the inner ear, where the normal processes act tocomplete the hearing process. Bone conduction is used as ameans of diagnosing hearing disorders that may arise be-cause of lesions in the ossicular chain. Some hearing aidsemploy bone conduction to overcome such deficits.

The Inner Ear. The actual process of sound transductiontakes place in the inner ear, where the sensory receptorsand their neural connections are located. The relationshipbetween its structure and function is a close and complexone. The following discussion includes the most significantaspects of this relationship.

Overall Structure. The auditory structures are locatedin the cochlea (Fig. 4.19), part of a cavity in the temporalbone called the bony labyrinth. The cochlea (meaning“snail shell”) is a fluid-filled spiral tube that arises from a


The cochlea and the organ of Corti. Left:An overview of the membranous labyrinth of

the cochlea. Upper right: A cross section through one turn of thecochlea, showing the canals and membranes that make up thestructures involved in the final processes of auditory sensation.

FIGURE 4.19 Lower right: An enlargement of a cross section of the organ ofCorti, showing the relationships among the hair cells and themembranes. (Modified from Gulick WL, Gescheider GA, FrisinaRD. Hearing: Physiological Acoustics, Neural Coding, and Psy-choacoustics. New York: Oxford University Press, 1989.)


cavity called the vestibule, with which the organs of bal-ance also communicate. In the human ear, the cochlea isabout 35 mm long and makes about 23/4 turns. Togetherwith the vestibule it contains a total fluid volume of 0.1 mL.It is partitioned longitudinally into three divisions (canals)called the scala vestibuli (into which the oval windowopens), the scala tympani (sealed off from the middle earby the round window), and the scala media (in which thesensory cells are located). Arising from the bony center axisof the spiral (the modiolus) is a winding shelf called the os-seous spiral lamina; opposite it on the outer wall of the spi-ral is the spiral ligament, and connecting these two struc-tures is a highly flexible connective tissue sheet, the basilarmembrane, that runs for almost the entire length of thecochlea. The basilar membrane separates the scala tympani(below) from the scala media (above). The hair cells, whichare the actual sensory receptors, are located on the uppersurface of the basilar membrane. They are called hair cellsbecause each has a bundle of hair-like cilia at the end thatprojects away from the basilar membrane.

Reissner’s membrane, a delicate sheet only two cell lay-ers thick, divides the scala media (below) from the scalavestibuli (above) (see Fig. 4.19). The scala vestibuli com-municates with the scala tympani at the apical (distal) endof the cochlea via the helicotrema, a small opening wherea portion of the basilar membrane is missing. The scalavestibuli and scala tympani are filled with perilymph, a fluidhigh in sodium and low in potassium. The scala media con-tains endolymph, a fluid high in potassium and low insodium. The endolymph is secreted by the stria vascularis,a layer of fibrous vascular tissue along the outer wall of thescala media. Because the cochlea is filled with incompress-ible fluid and is encased in hard bone, pressure changescaused by the in-and-out motion at the oval window(driven by the stapes) are relieved by an out-and-in motionof the flexible round window membrane.

Sensory Structures. The organ of Corti is formed bystructures located on the upper surface of the basilar mem-brane and runs the length of the scala media (see Fig. 4.19).It contains one row of some 3,000 inner hair cells; the archof Corti and other specialized supporting cells separate theinner hair cells from the three or four rows of outer haircells (about 12,000) located on the stria vascularis side. Therows of inner and outer hair cells are inclined slightly to-ward each other and covered by the tectorial membrane,which arises from the spiral limbus, a projection on the up-per surface of the osseous spiral lamina.

Nerve fibers from cell bodies located in the spiral gan-glia form radial bundles on their way to synapse with theinner hair cells. Each nerve fiber makes synaptic connec-tion with only one hair cell, but each hair cell is served by8 to 30 fibers. While the inner hair cells comprise only 20%of the hair cell population, they receive 95% of the afferentfibers. In contrast, many outer hair cells are each served bya single external spiral nerve fiber. The collected afferentfibers are bundled in the cochlear nerve, which exits the in-ner ear via the internal auditory meatus. Some efferentfibers also innervate the cochlea. They may serve to en-hance pitch discrimination and the ability to distinguishsounds in the presence of noise. Recent evidence suggeststhat efferent fibers to the outer hair cells may cause them to

shorten (contract), altering the mechanical properties ofthe cochlea.

The Hair Cells. The hair cells of the inner and the outerrows are similar anatomically. Both sets are supported andanchored to the basilar membrane by Deiters’ cells and ex-tend upward into the scala media toward the tectorial mem-brane. Extensions of the outer hair cells actually touch thetectorial membrane, while those of the inner hair cells ap-pear to stop just short of contact. The hair cells makesynaptic contact with afferent neurons that run throughchannels between Deiters’ cells. A chemical transmitter ofunknown identity is contained in synaptic vesicles near thebase of the hair cells; as in other synaptic systems, the en-try of calcium ions (associated with cell membrane depo-larization) is necessary for the migration and fusion of thesynaptic vesicles with the cell membrane prior to transmit-ter release.

At the apical end of each inner hair cell is a projectingbundle of about 50 stereocilia, rod-like structures packed inthree, parallel, slightly curved rows. Minute strands link thefree ends of the stereocilia together, so the bundle tends tomove as a unit. The height of the individual stereocilia in-creases toward the outer edge of the cell (toward the striavascularis), giving a sloping appearance to the bundle.Along the cochlea, the inner hair cells remain constant insize, while the stereocilia increase in height from about 4�m at the basal end to 7 �m at the apical end. The outer haircells are more elongated than the inner cells, and their sizeincreases along the cochlea from base to apex. Their stere-ocilia (about 100 per hair cell) are also arranged in threerows that form an exaggerated W figure. The height of thestereocilia also increases along the length of the cochlea,and they are embedded in the tectorial membrane. Thestereocilia of both types of hair cells extend from the cutic-ular plate at the apex of the cell. The diameter of an indi-vidual stereocilium is uniform (about 0.2 �m) except at thebase, where it decreases significantly. Each stereociliumcontains cross-linked and closely packed actin filaments,and, near the tip, is a cation-selective transduction channel.

Mechanical transduction in hair cells is shown in Figure4.20. When a hair bundle is deflected slightly (the thresh-old is less than 0.5 nm) toward the stria vascularis, minutemechanical forces open the transduction channels, andcations (mostly potassium) enter the cells. The resultingdepolarization, roughly proportional to the deflection,causes the release of transmitter molecules, generating af-ferent nerve action potentials. Approximately 15% of thetransduction channels are open in the absence of any de-flection, and bending in the direction of the modiolus ofthe cochlea results in hyperpolarization, increasing therange of motion that can be sensed. Hair cells are quite in-sensitive to movements of the stereocilia bundles at rightangles to their preferred direction.

The response time of hair cells is remarkable; they candetect repetitive motions of up to 100,000 times per sec-ond. They can, therefore, provide information throughoutthe course of a single cycle of a sound wave. Such rapid re-sponse is also necessary for the accurate localization ofsound sources. When a sound comes from directly in frontof a listener, the waves arrive simultaneously at both ears. Ifthe sound originates off to one side, it reaches one ear

sooner than the other and is slightly more intense at thenearer ear. The difference in arrival time is on the order oftenths of a millisecond, and the rapid response of the haircells allows them to provide temporal input to the auditorycortex. The timing and intensity information are processedin the auditory cortex into an accurate perception of the lo-cation of the sound source.

Integrated Function of the Organ of Corti. The actualtransduction of sound requires an interaction among thetectorial membrane, the arches of Corti, the hair cells, andthe basilar membrane. When a sound wave is transmitted tothe oval window by the ossicular chain, a pressure wavetravels up the scala vestibuli and down the scala tympani(Fig. 4.21). The canals of the cochlea, being encased inbone, are not deformed, and movements of the round win-dow allow the small volume change needed for the trans-mission of the pressure wave. Resulting eddy currents in thecochlear fluids produce an undulating distortion in thebasilar membrane. Because the stiffness and width of themembrane vary with its length (it is wider and less stiff atthe apex than at the base), the membrane deformation takesthe form of a “traveling wave,” which has its maximal am-plitude at a position along the membrane corresponding tothe particular frequency of the sound wave (Fig. 4.22).Low-frequency sounds cause a maximal displacement of themembrane near its apical end (near the helicotrema),whereas high-frequency sounds produce their maximal ef-fect at the basal end (near the oval window). As the basilarmembrane moves, the arches of Corti transmit the move-

ment to the tectorial membrane, the stereocilia of the outerhair cells (embedded in the tectorial membrane) are sub-jected to lateral shearing forces that stimulate the cells, andaction potentials arise in the afferent neurons.

Because of the tuning effect of the basilar membrane,only hair cells located at a particular place along the mem-brane are maximally stimulated by a given frequency(pitch). This localization is the essence of the place theoryof pitch discrimination, and the mapping of specific tones(pitches) to specific areas is called tonotopic organization.As the signals from the cochlea ascend through the com-plex pathways of the auditory system in the brain, the tono-topic organization of the neural elements is at least partiallypreserved, and pitch can be spatially localized throughoutthe system. The sense of pitch is further sharpened by theresonant characteristics of the different-length stereociliaalong the length of the cochlea and by the frequency-re-sponse selectivity of neurons in the auditory pathway. Thecochlea acts as both a transducer for sound waves and a fre-quency analyzer that sorts out the different pitches so they


Mechanical transduction in the hair cells of

the ear. A, Deflection of the stereocilia opensapical K� channels. B, The resulting depolarization allows theentry of Ca2� at the basal end of the cell. This causes the releaseof the neurotransmitter, thereby exciting the afferent nerve.(Adapted from Hudspeth AJ. The hair cells of the inner ear. SciAm 1983;248(1):54–64.)

FIGURE 4.20

The mechanics of the cochlea, showing the

action of the structures responsible for

pitch discrimination (with only the basilar membrane of the

organ of Corti shown). When the compression phase of asound wave arrives at the eardrum, the ossicles transmit it to theoval window, which is pushed inward. A pressure wave travels upthe scala vestibuli and (via the helicotrema) down the scala tym-pani. To relieve the pressure, the round window membrane bulgesoutward. Associated with the pressure waves are small eddy cur-rents that cause a traveling wave of displacement to move alongthe basilar membrane from base to apex. The arrival of the nextrarefaction phase reverses these processes. The frequency of thesound wave, interacting with the differences in the mass, width,and stiffness of the basilar membrane along its length, determinesthe characteristic position at which the membrane displacementis maximal. This localization is further detailed in Figure 4.22.

FIGURE 4.21


can be separately distinguished. In the midrange of hearing(around 1,000 Hz), the human auditory system can sense adifference in frequency of as little as 3 Hz. The tonotopicorganization of the basilar membrane has facilitated the in-vention of prosthetic devices whose aim is to provide somereplacement of auditory function to people suffering fromdeafness that arises from severe malfunction of the middleor inner ear (see Clinical Focus Box 4.1).

Central Auditory Pathways. Nerve fibers from thecochlea enter the spiral ganglion of the organ of Corti;from there, fibers are sent to the dorsal and ventralcochlear nuclei. The complex pathway that finally ends atthe auditory cortex in the superior portion of the temporallobe of the brain involves several sets of synapses and con-siderable crossing over and intermediate processing. Aswith the eye, there is a spatial correlation between cells inthe sensory organ and specific locations in the primary au-ditory cortex. In this case, the representation is called atonotopic map, with different pitches being represented bydifferent locations, even though the firing rates of the cells

no longer correspond to the frequency of sound originallypresented to the inner ear.

The Function of the Vestibular Apparatus. The ear alsohas important nonauditory sensory functions. The sensoryreceptors that allow us to maintain our equilibrium and bal-ance are located in the vestibular apparatus, which consists(on each side of the head) of three semicircular canals andtwo otolithic organs, the utricle and the saccule (Fig.4.23). These structures are located in the bony labyrinth ofthe temporal bone and are sometimes called the membra-nous labyrinth. As with hearing, the basic sensing elementsare hair cells.

The semicircular canals, hoop-like tubular membranousstructures, sense rotary acceleration and motion. Their in-terior is continuous with the scala media and is filled withendolymph; on the outside, they are bathed by perilymph.The three canals on each side lie in three mutually perpen-dicular planes. With the head tipped forward by about 30degrees, the horizontal (lateral) canal lies in the horizontalplane. At right angles to this are the planes of the anterior

Membrane localization of different frequen-

cies. A, The upper portion shows a travelingwave of displacement along the basilar membrane at two instants.Over time, the peak excursions of many such waves form an enve-lope of displacement with a maximal value at about 28 mm fromthe stapes (lower portion); at this position, its stimulating effect

FIGURE 4.22 on the hair cells will be most intense. B, The effect of frequency.Lower frequencies produce a maximal effect at the apex of thebasilar membrane, where it is the widest and least stiff. Pure tonesaffect a single location; complex tones affect multiple loci. (Modi-fied from von Békésy G. Experiments in Hearing. New York: Mc-Graw-Hill, 1960.)

with the posterior canal on the other side, and the twofunction as a pair. The horizontal canals also lie in a com-mon plane.

Near its junction with the utricle, each canal has aswollen portion called the ampulla. Each ampulla containsa crista ampullaris, the sensory structure for that semicir-cular canal; it is composed of hair cells and supporting cellsencapsulated by a cupula, a gelatinous mass (Fig. 4.24).The cupula extends to the top of the ampulla and is movedback and forth by movements of the endolymph in thecanal. This movement is sensed by displacement of thestereocilia of the hair cells. These cells are much like thoseof the organ of Corti, except that at the “tall” end of thestereocilia array there is one larger cilium, the kinocilium.All the hair cells have the same orientation. When thestereocilia are bent toward the kinocilium, the frequency ofaction potentials in the afferent neurons leaving the am-pulla increases; bending in the other direction decreasesthe action potential frequency.

The role of the semicircular canals in sensing rotary ac-celeration is shown on the left side of Figure 4.25. Themechanisms linking stereocilia deflection to receptor po-tentials and action potential generation are quite similar tothose in the auditory hair cells. Because of the inertia of theendolymph in the canals, when the position of the head ischanged, fluid currents in the canals cause the deflection of


CLINICAL FOCUS BOX 4.1

Cochlear Implants

Disorders of hearing are broadly divided into the cate-gories of conductive hearing loss, related to structuresof the outer and middle ear; sensorineural hearing loss(“nerve deafness”), dealing with the mechanisms of thecochlea and peripheral nerves; and central hearing loss,concerning processes that lie in higher portions of the cen-tral nervous system.

Damage to the cochlea, especially to the hair cells of theorgan of Corti, produces sensorineural hearing loss by sev-eral means. Prolonged exposure to loud occupational orrecreational noises can lead to hair cell damage, includingmechanical disruption of the stereocilia. Such damage islocalized in the outer hair cells along the basilar membraneat a position related to the pitch of the sound that producedit. Antibiotics such as streptomycin and certain diureticscan cause rapid and irreversible damage to hair cells simi-lar to that caused by noise, but it occurs over a broad rangeof frequencies. Diseases such as meningitis, especially inchildren, can also lead to sensorineural hearing loss.

In carefully selected patients, the use of a cochlear im-plant can restore some function to the profoundly deaf.The device consists of an external microphone, amplifier,and speech processor coupled by a plug-and-socket con-nection, magnetic induction, or a radio frequency link to areceiver implanted under the skin over the mastoid bone.Stimulating wires then lead to the cochlea. A single extra-cochlear electrode, applied to the round window, can re-store perception of some environmental sounds and aid inlip-reading, but it will not restore pitch or speech discrimi-nation. A multielectrode intracochlear implant (withup to 22 active elements spaced along it) can be insertedinto the basal turn of the scala tympani. The linear spatial

arrangement of the electrodes takes advantage of thetonotopic organization of the cochlea, and some pitch (fre-quency) discrimination is possible. The external processorseparates the speech signal into several frequency bandsthat contain the most critical speech information, and themultielectrode assembly presents the separated signals tothe appropriate locations along the cochlea. In some de-vices the signals are presented in rapid sequence, ratherthan simultaneously, to minimize interference between ad-jacent areas.

When implanted successfully, such a device can restoremuch of the ability to understand speech. Considerabletraining of the patient and fine-tuning of the speechprocessor are necessary. The degree of restoration of func-tion ranges from recognition of critical environmentalsounds to the ability to converse over a telephone.Cochlear implants are most successful in adults who be-came deaf after having learned to speak and hear natu-rally. Success in children depends critically on their ageand linguistic ability; currently, implants are being used inchildren as young as age 2.

Infrequent problems with infection, device failure, andnatural growth of the auditory structures may limit the use-fulness of cochlear implants for some patients. In certaincases, psychological and social considerations may dis-courage the advisability of using of auditory prosthetic de-vices in general. From a technical standpoint, however,continual refinements in the design of implantable devicesand the processing circuitry are extending the range ofsubjects who may benefit from cochlear implants. Re-search directed at external stimulation of higher auditorystructures may eventually lead to even more effectivetreatments for profound hearing loss.

The vestibular apparatus in the bony

labyrinth of the inner ear. The semicircularcanals sense rotary acceleration and motion, while the utricle andsaccule sense linear acceleration and static position.

FIGURE 4.23

vertical (superior) canal and the posterior vertical canal,which are perpendicular to each other. The planes of theanterior vertical canals are each at approximately 45� to themidsagittal section of the head (and at 90� to each other).Thus, the anterior canal on one side lies in a plane parallel


the cupula and the hair cells are stimulated. The fluid cur-rents are roughly proportional to the rate of change of ve-locity (i.e., to the rotary acceleration), and they result in aproportional increase or decrease (depending on the direc-tion of head rotation) in action potential frequency. As a re-sult of the bilateral symmetry in the vestibular system, canalswith opposite pairing produce opposite neural effects. Thevestibular division of cranial nerve VIII passes the impulsesfirst to the vestibular ganglion, where the cell bodies of theprimary sensory neurons lie. The information is then passedto the vestibular nuclei of the brainstem and from there tovarious locations involved in sensing, correcting, and com-pensating for changes in the motions of the body.

The remaining vestibular organs, the saccule and the utri-cle, are also part of the membranous labyrinth. They com-municate with the semicircular canals, the cochlear duct,and the endolymphatic duct. The sensory structures in theseorgans, called maculae, also employ hair cells, similar tothose of the ampullar cristae (Fig. 4.26). The macular haircells are covered with the otolithic membrane, a gelatinoussubstance in which are embedded numerous small crystals ofcalcium carbonate called otoliths (otoconia). Because theotoliths are heavier than the endolymph, tilting of the headresults in gravitational movement of the otolithic membraneand a corresponding change in sensory neuron action po-tential frequency. As in the ampulla, the action potential fre-quency increases or decreases depending on the direction ofdisplacement. The maculae are adapted to provide a steadysignal in response to displacement; in addition, they are lo-cated away from the semicircular canals and are not subjectto motion-induced currents in the endolymph. This allowsthem to monitor the position of the head with respect to a

steady gravitational field. The maculae also respond pro-portionally to linear acceleration.

The vestibular apparatus is an important component inseveral reflexes that serve to orient the body in space andmaintain that orientation. Integrated responses to

The sensory structure of the semicircular

canals. A, The crista ampularis contains thehair (receptor) cells, and the whole structure is deflected by mo-tion of the endolymph. B, An individual hair cell.

FIGURE 4.24

Slow eyemovements

Slowmovement

Slowmovement

Head rotation

The role of the semicircular canals in sens-

ing rotary acceleration. This sensation islinked to compensatory eye movements by the vestibuloocular re-flex. Only the horizontal canals are considered here. This pair ofcanals is shown as if one were looking down through the top of ahead looking toward the top of the page. Within the ampulla ofeach canal is the cupula, an extension of the crista ampullaris, thestructure that senses motion in the endolymph fluid in the canal.Below each canal is the action potential train recorded from thevestibular nerve. A, The head is still, and equal nerve activity isseen on both sides. There are no associated eye movements (rightcolumn). B, The head has begun to rotate to the left. The inertiaof the endolymph causes it to lag behind the movement, produc-ing a fluid current that stimulates the cupulae (arrows show thedirection of the relative movements). Because the two canals aremirror images, the neural effects are opposite on each side (thecupulae are bent in relatively opposite directions). The reflex ac-tion causes the eyes to move slowly to the right, opposite to thedirection of rotation (right column); they then snap back and be-gin the slow movement again as rotation continues. The fastmovement is called rotatory nystagmus. C, As rotation continues,the endolymph “catches up” with the canal because of fluid fric-tion and viscosity, and there is no relative movement to deflectthe cupulae. Equal neural output comes from both sides, and theeye movements cease. D, When the rotation stops, the inertia ofthe endolymph causes a current in the same direction as the pre-ceding rotation, and the cupulae are again deflected, this time in amanner opposite to that shown in part B. The slow eye move-ments now occur in the same direction as the former rotation.

FIGURE 4.25

vestibular sensory input include balancing and steadyingmovements controlled by skeletal muscles, along withspecific reflexes that automatically compensate for bod-ily motions. One such mechanism is the vestibuloocularreflex. If the body begins to rotate and, thereby, stimu-late the horizontal semicircular canals, the eyes will moveslowly in a direction opposite to that of the rotation andthen suddenly snap back the other way (see Fig. 4.25,right). This movement pattern, called rotatory nystag-mus, aids in visual fixation and orientation and takesplace even with the eyes closed. It functions to keep theeyes fixed on a stationary point (real or imaginary) as thehead rotates. By convention, the direction of the rapideye movement is used to label the direction of the nys-tagmus, and this movement is in the same direction as therotation. As rotation continues, the relative motion of theendolymph in the semicircular canals ceases, and the nys-tagmus disappears. When rotation stops, the inertia ofthe endolymph causes it to continue in motion and againthe cupulae are displaced, this time from the opposite di-rection. The slow eye movements are now in the same di-rection as the prior rotation; the postrotatory nystagmus(fast phase) that develops is in a direction opposite to theprevious rotation. As long as the endolymph continues itsrelative movement, the nystagmus (and the sensation ofrotary motion) persists. Irrigation of the ear with waterabove or below body temperature causes convection cur-rents in the endolymph. The resulting unilateral caloricstimulation of the semicircular canal produces symptomsof vertigo, nystagmus, and nausea. Disturbances of thelabyrinthine function produce the symptoms of vertigo,a disorder that can significantly affect daily activities (seeClinical Focus Box 4.2).

Related mechanisms involving the otolithic organs pro-duce automatic compensations (via the postural and ex-traocular musculature) when the otolithic organs are stimu-lated by transient or maintained changes in the position ofthe head. If the otolithic organs are stimulated rhythmi-cally, as by the motion of a ship or automobile, the dis-tressing symptoms of motion sickness (vertigo, nausea,

sweating, etc.) may appear. Over time, these symptomslessen and disappear.

The Special Chemical Senses Detect Molecules

in the Environment

Chemical sensation includes not only the special chemicalsenses described below, but also internal sensory receptorfunctions that monitor the concentrations of gases andother chemical substances dissolved in the blood or otherbody fluids. Since we are seldom aware of these internalchemical sensations, they are treated throughout this bookas needed; the discussion here covers only taste and smell.

Gustatory Sensation. The sense of taste is mediated bymulticellular receptors called taste buds, several thousandof which are located on folds and projections on the dorsaltongue, called papillae. Taste buds are located mainly onthe tops of the numerous fungiform papillae but are also lo-cated on the sides of the less numerous foliate and vallatepapillae. The filiform papillae, which cover most of thetongue, usually do not bear taste buds. An individual tastebud is a spheroid collection of about 50 individual cells thatis about 70 �m high and 40 �m in diameter (Fig. 4.27). Thecells of a taste bud lie mostly buried in the surface of thetongue, and materials access the sensory cells by way of thetaste pore.

Most of the cells of a taste bud are sensory cells. At theirapical ends, they are connected laterally by tight junctions,and they bear microvilli that greatly increase the surfacearea they present to the environment. At their basal ends,they form synapses with the facial (VII) and glossopharyn-geal (IX) cranial nerves. This arrangement indicates thatthe sensory cells are actually secondary receptors (like thehair cells of the ear), since they are anatomically separatefrom the afferent sensory nerves. About 50 afferent fibersenter each taste bud, where they branch so that each axonsynapses with more than one sensory cell. Among the sen-sory cells are elongated supporting cells that do not havesynaptic connections. The sensory cells typically have alifespan of 10 days. They are continually replenished bynew sensory cells formed from the basal cells of the lowerpart of the taste buds. When a sensory cell is replaced by amaturing basal cell, the old synaptic connections are bro-ken, and new ones must be formed.

From the point of view of their receptors, the traditionalfour modalities of taste—sweet, sour, salty, and bitter—are well defined, and the areas of the tongue where they arelocated are also rather specific, although the degree of lo-calization depends on the concentration of the stimulatingsubstance. In general, the receptors for sweetness are lo-cated just behind the tip of the tongue, sour receptors arelocated along the sides, the salt sensation is localized at thetip, and the bitter sensation is found across the rear of thetongue. (The two “accessory qualities” of taste sensation arealkaline [soapy] and metallic.) The broad surface of thetongue is not as well supplied with taste buds. Most tasteexperiences involve several different sensory modalities, in-cluding taste, smell, mechanoreception (for texture), andtemperature; artificially confining the taste sensation toonly the four modalities found on the tongue (e.g., by


The relation of the otoliths to the sensory

cells in the macula of the utricle and sac-

cule. The gravity-driven movement of the otoliths stimulates thehair cells.

FIGURE 4.26


blocking the sense of smell) greatly diminishes the range oftaste perceptions.

Recent studies have provided evidence for a fifth tastemodality, one that is called umami, or savoriness. Its recep-tors are stimulated quite specifically by glutamate ions,which are contained in naturally occurring dietary proteinand are responsible for a “meaty” taste. Glutamate ions can

also be provided as a flavor-enhancer in the well-knownfood additive MSG, monosodium glutamate.

While the functional receptor categories are well de-fined, it is much more difficult to determine what kind ofstimulating chemical will produce a given taste sensation.Chemicals that produce a sour sensation are usually acids,and the intensity of the perception depends on the degree

CLINICAL FOCUS BOX 4.2

Vertigo

A common medical complaint is dizziness. This symptommay be a result of several factors, such as cerebral is-chemia (“feeling faint”), reactions to medication, distur-bances in gait, or disturbances in the function of thevestibular apparatus and its central nervous system con-nections. Such disturbances can produce the phenomenonof vertigo, which may be defined as the illusion of motion(usually rotation) when no motion is actually occurring.Vertigo is often accompanied by autonomic nervous sys-tem symptoms of nausea, vomiting, sweating, and pallor.

The body uses three integrated systems to establish itsplace in space: the vestibular system, which senses posi-tion and rotation of the head; the visual system, which pro-vides spatial information about the external environment;and the somatosensory system, which provides informa-tion from joint, skin, and muscle receptors about limb po-sition. Several forms of vertigo can arise from distur-bances in these systems. Physiological vertigo canresult when there is discordant input from the three sys-tems. Seasickness results from the unaccustomed repeti-tive motion of a ship (sensed via the vestibular system).Rapidly changing visual fields can cause visually-inducedmotion sickness, and space sickness is associated withmultiple-input disturbances. Central positional vertigocan arise from lesions in cranial nerve VIII (as may be as-sociated with multiple sclerosis or some tumors), verte-brovascular insufficiency (especially in older adults), orfrom impingement of vascular loops on neural structures.It is commonly present with other CNS symptoms. Pe-ripheral vertigo arises from disturbances in the vestibu-lar apparatus itself. The problem may be either unilateralor bilateral. Causes include trauma, physical defects in thelabyrinthine system, and pathological syndromes such asMénière’s disease. As in the cochlea, aging produces con-siderable hair cell loss in the cristae and maculae of thevestibular system. Caloric stimulation can be used as an in-dicator of the degree of vestibular function.

The most common form of peripheral vertigo is benignparoxysmal positional vertigo (BPPV). This is a severevertigo, with incidence increasing with age. Episodes ap-pear rapidly and are limited in duration (from minutes todays). They are usually brought on by assuming a particu-lar position of the head, such as one might do when paint-ing a ceiling. BPPV is thought to be due to the presence ofcanaliths, debris in the lumen of one of the semicircularcanals. The offending particles are usually clumps of oto-conia (otoliths) that have been shed from the maculae ofthe saccule and utricle, whose passages are connected tothe semicircular canals. These clumps act as gravity-drivenpistons in the canals, and their movement causes the en-dolymph to flow, producing the sensation of rotary mo-tion. Because they are in the lowest position, the posteriorcanals are the most frequently affected. In addition to the

rotating sensation, this input gives rise, via the vestibu-loocular system, to a pattern of nystagmus (eye move-ments) appropriate to the spurious input.

The specific site of the problem can be determined byusing the Dix-Hallpike maneuver, which is a series ofphysical maneuvers (changes in head and body position).By observing the resulting pattern of nystagmus and re-ported symptoms, the location of the defect can be de-duced. Another set of maneuvers known as the canalithrepositioning procedure of Epley can cause gravity tocollect the loose canaliths and deposit them away from thelumen of the semicircular canal. This procedure is highlyeffective in cases of true BPPV, with a cure rate of up to85% on the first attempt and nearly 100% on a subsequentattempt. Patients can be taught to perform the procedureon themselves if the problem returns.

Ménière’s disease is a syndrome of uncertain (but pe-ripheral) origin associated with vertigo. Its cause(s) andprecipitating factors are not well understood. Typical asso-ciated findings include fluctuating hearing loss and tinni-tus (ringing in the ears). Episodes involve increased fluidpressure in the labyrinthine system, and symptoms maydecrease in response to salt restriction and diuretics. Othercases of peripheral vertigo may be caused by trauma (usu-ally unilateral) or by toxins or drugs (such as some antibi-otics); this type is often bilateral.

Central and peripheral vertigo may often be differenti-ated on the basis of their specific symptoms. Peripheralvertigo is more severe, and its nystagmus shows a delay(latency) in appearing after a position change. Its nystag-mus fatigues and can be reduced by visual fixation. Posi-tion sensitive and of finite duration, the condition usuallyinvolves a horizontal orientation. Central vertigo, usuallyless severe, shows a vertically oriented nystagmus withoutlatency and fatigability; it is not suppressed by visual fixa-tion and may be of long duration.

Treatment for vertigo, beyond that mentioned above,can involve bed rest and vestibular inhibiting drugs (suchas some antihistamines). However, these treatments arenot always effective and may delay the natural compensa-tion that can be aided by physical motion, such as walking(unpleasant as that may be). In severe cases that requiresurgical intervention (labyrinthectomy, etc.), patients canoften achieve a workable position sense via the other sen-sory inputs involved in maintaining equilibrium. Some ac-tivities, such as underwater swimming, must be avoidedby those with an impaired sense of orientation, since falsecues may lead to moving in inappropriate directions andincrease the risk of drowning.

References

Baloh RW. Vertigo. Lancet 1998;352:1841–1846.Furman JM, Cass SP. Primary care: Benign paroxysmal po-sitional vertigo. N Engl J Med 1999;341:1590–1596.

of dissociation of the acid (i.e., the number of free hydro-gen ions). Most sweet substances are organic; sugars, espe-cially, tend to produce a sweet sensation, although thresh-olds vary widely. For example, sucrose is about 8 times assweet as glucose. By comparison, the apparent sweetness ofsaccharin, an artificial sweetener, is 600 times as great asthat of sucrose, although it is not a sugar. Unfortunately,the salts of lead are also sweet, which can lead to ingestionof toxic levels of this poisonous metal. Substances produc-ing a bitter taste form a heterogeneous group. The classicbitter substance is quinine; nicotine and caffeine are alsobitter, as are many of the salts of calcium, magnesium, andammonium, the bitter taste being due to the cation portionof the salt. Sodium ions produce a salty sensation; some or-ganic compounds, such as lysyltaurine, are even more po-tent in this regard than sodium chloride.

The intensity of a taste sensation depends on the con-centration of the stimulating substance, but application ofthe same concentration to larger areas of the tongue pro-duces a more intense sensation; this is probably due to fa-cilitation involving a greater number of afferent fibers.Some taste sensations also increase with time, althoughtaste receptors show a slow but definite adaptation. Ele-vated temperature, over some ranges, tends to increase theperceived taste intensity, while dilution by saliva and seroussecretions from the tongue decreases the intensity. Thespecificity of the taste sensation arising from a particularstimulating substance results from the effects of specific re-ceptor molecules on the microvilli of the sensory cells.Salty substances probably depolarize sensory cells directly,while sour substances may produce depolarization byblocking potassium channels with hydrogen ions. Bitter

substances bind to specific G protein-coupled receptorsand activate phospholipase C to increase the cell concen-tration of inositol trisphosphate, which promotes calciumrelease from the endoplasmic reticulum. Sweet substancesalso act through G protein-coupled receptors and cause in-creases in adenylyl cyclase activity, increasing cAMP,which, in turn, promotes the phosphorylation of membranepotassium channels. The resulting decrease in potassiumconductance leads to depolarization. In the case of theumami taste, there is evidence of specific G protein-cou-pled receptors in the cell membranes of sensory taste cells.

Olfactory Sensation. Compared with that of many otheranimals, the human sense of smell is not particularly acute.Nevertheless, we can distinguish 2,000 to 4,000 differentodors that cover a wide range of chemical species. The re-ceptor organ for olfaction is the olfactory mucosa, an areaof approximately 5 cm2 located in the roof of the nasal cav-ity. Normally there is little air flow in this region of thenasal tract, but sniffing serves to direct air upward, increas-ing the likelihood of an odor being detected.

The olfactory mucosa contains about 10 to 20 millionreceptor cells. In contrast to the taste sensory cells, the ol-factory cells are neurons and, as such, are primary recep-tors. These cells are interspersed among supporting (sus-tentacular) cells, and tight junctions bind the cellstogether at their sensory ends (Fig. 4.28). The receptor


Supportingcell

Synapse

Afferent fibers

Sensorycell

Basalcell

Tight junctionMicrovilliEpithelium

Taste pore

The sensory and supporting cells in a taste

bud. The afferent nerve synapse with the basalareas of the sensory cells. (Modified from Schmidt RF, ed. Funda-mentals of Sensory Physiology. 2nd Ed. New York: Springer-Ver-lag, 1981.)

FIGURE 4.27

Fila olfactoria(axons)

CiliaOlfactory rod(dendrite)

Tightjunction

Receptorcell

Supportingcell

Basement membrane

The sensory cells in the olfactory mucosa.

The fila olfactoria, the axons leading from thereceptor cells, are part of the sensory cells, in contrast to thesituation in taste receptors. (Modified from Ganong WF. Re-view of Medical Physiology. 20th Ed. Stamford, CT: McGraw-Hill, 2001.)

FIGURE 4.28


cells terminate at their apical ends with short, thick den-drites called olfactory rods, and each cell bears 10 to 20cilia that extend into a thin covering of mucus secreted byBowman’s glands located throughout the olfactory mucosa.Molecules to be sensed must be dissolved in this mucouslayer. The basal ends of the receptor cells form axonalprocesses called fila olfactoria that pass through the cribri-form plate of the ethmoid bone. These short axons synapsewith the mitral cells in complex spherical structures calledolfactory glomeruli located in the olfactory bulb, part ofthe brain located just above the olfactory mucosa. Here thecomplex afferent and efferent neural connections for the ol-factory tract are made. Approximately 1,000 fila olfactoriasynapse on each mitral cell, resulting in a highly conver-gent relationship. Lateral connections are also plentiful inthe olfactory bulb, which also contains efferent fibersthought to have an inhibitory function.

The olfactory mucosa also contains sensory fibers fromthe trigeminal (V) cranial nerve. They are sensitive to cer-tain odorous substances, such as peppermint and chlorine,and play a role in the initiation of reflex responses (e.g.,sneezing) that result from irritation of the nasal tract.

The modalities of smell are numerous and do not fallinto convenient classes, though some general categories,such as flowery, sweaty, or rotten, may be distinguished.

Olfactory thresholds vary widely from substance to sub-stance; the threshold concentration for the detection ofethyl ether is around 5.8 mg/L air, while that for methylmercaptan (the odor of garlic) is approximately 0.5 ng/L.This represents a 10 million-fold difference in sensitivity.The basis for odor discrimination is not well understood. Itis not likely that there is a receptor molecule for every pos-sible odor substance located in the membranes of the ol-factory cilia, and it appears that complex odor sensationsarise from unique spatial patterns of activation throughoutthe olfactory mucosa.

Signal transduction appears to involve the binding ofa molecule of an odorous substance to a G protein-cou-pled receptor on a cilium of a sensory cell. This bindingcauses the production of cAMP that binds to, and opens,sodium channels in the ciliary membrane. The resultinginward sodium current depolarizes the cell to produce agenerator potential, which causes action potentials toarise in the initial segments of the fila olfactoria. Thesense of smell shows a high degree of adaptation, some ofwhich takes place at the level of the generator potentialand some of which may be due to the action of efferentneurons in the olfactory bulb. Discrimination betweenodor intensities is not well defined; detectable differ-ences may be about 30%.

DIRECTIONS: Each of the numbereditems or incomplete statements in thissection is followed by answers orcompletions of the statement. Select theONE lettered answer or completion that isBEST in each case.

1. An increase in the action potentialfrequency in a sensory nerve usuallysignifies(A) Increased intensity of the stimulus(B) Cessation of the stimulus(C) Adaptation of the receptor(D) A constant and maintainedstimulus(E) An increase in the action potentialconduction velocity

2. Why is the blind spot on the retina notusually perceived?(A) It is very small, below the ability ofthe sensory cells to detect(B) It is present only in very youngchildren(C) Its location in the visual field isdifferent in each eye(D) Constant eye motion prevents thespot from remaining still(E) Lateral input from adjacent cellsfills in the missing information

3. The condition known as presbyopia isdue to(A) Change in the shape of the eyeballas a result of age

(B) An age-related loss of cells in theretina(C) Change in the elasticity of the lensas a result of age(D) A loss of transparency in the lens(E) Increased opacity of the vitreoushumor

4. What external aids can be used to helpa myopic eye compensate for distancevision?(A) A positive (converging) lens placedin front of the eye(B) A negative (diverging) lens placedin front of the eye(C) A cylindrical lens placed in frontof the eye(D) Eyeglasses that are partiallyopaque, to reduce the light intensity(E) No help is needed because the eyeitself can accommodate

5. At which location along the basilarmembrane are the highest-frequencysounds detected?(A) Nearest the oval window(B) Farthest from the oval window,near the helicotrema(C) Uniformly along the basilarmembrane(D) At the midpoint of the membrane(E) At a series of widely-spacedlocations along the membrane

6. Motion of the endolymph in thesemicircular canals when the head is

held still will result in the perceptionof(A) Being upside-down(B) Moving in a straight line(C) Continued rotation(D) Being upright and stationary(E) Lying on one’s back

7. A decrease in sensory response while astimulus is maintained constant is dueto the phenomenon of(A) Adaptation(B) Fatigue(C) The graded response(D) Compression

8. Sensory receptors that adapt rapidlyare well suited to sensing(A) The weight of an object held inthe hand(B) The rate at which an extremity isbeing moved(C) Resting body orientation in space(D) Potentially hazardous chemicals inthe environment(E) The position of an extended limb

9. Adaptation in a sensory receptor isassociated with a(A) Decline in the amplitude of actionpotentials in the sensory nerve(B) Reduction in the intensity of theapplied stimulus(C) Decline in the conduction velocityof sensory nerve action potentials

R E V I E W Q U E S T I O N S

(continued)


(D) Decline in the amplitude of thegenerator potential(E) Reduction in the duration of thesensory action potentials

10.Which of the following is the principalfunction of the bones (ossicles) of themiddle ear?(A) They provide mechanical supportfor the flexible membranes to whichthey are attached (i.e., the eardrum andthe oval window)(B) They reduce the amplitude of thevibrations reaching the oval window,protecting it from mechanical damage(C) They increase the efficiency ofvibration transfer through the middle ear(D) They control the opening of theeustachian tubes and allow pressures tobe equalized

(E) They have little effect on theprocess of hearing in humans, since they are essentially passivestructures

11.On a moonlit night, human vision ismonochromatic and less acute thanvision during the daytime. This isbecause(A) Objects are being illuminated bymonochromatic light, and there is noopportunity for color to be produced(B) The cone cells of the retina, whilemore closely packed than the rod cells,have a lower sensitivity to light of allcolors(C) Light rays of low intensity do notcarry information as to color(D) Retinal photoreceptor cells thathave become dark-adapted can no

longer respond to varying wavelengthsof light(E) At low light levels, the lens cannotaccommodate to sharpen vision

SUGGESTED READING

Ackerman D. A Natural History of theSenses. New York: Random House,1990.

Gulick WL, Gescheider GA, Frisina RD.Hearing: Physiological Acoustics,Neural Coding, and Psychoacoustics.New York: Oxford University Press,1989.

Hudspeth AJ. How hearing happens. Neu-ron 1997;19:947–950.

Spielman AI. Chemosensory function anddysfunction. Crit Rev Oral Biol Med1998;9:267–291.

PART II CHAPTER 4 Sensory Physiologyfac.ksu.edu.sa/sites/default/files/smch4.pdf · 2017-11-22 ·...

Documents

Transcript of PART II CHAPTER 4 Sensory Physiologyfac.ksu.edu.sa/sites/default/files/smch4.pdf · 2017-11-22 ·...