Three Types of Muscle Tissue 1.Skeletal muscle tissue: – Attached to bones and skin – Striated...

Three Types of Muscle Tissue

1. Skeletal muscle tissue:– Attached to bones and skin– Striated – Voluntary (i.e., conscious control)– Powerful– Primary topic of this chapter


2. Cardiac muscle tissue:– Only in the heart – Striated – Involuntary– More details in Chapter 18


3. Smooth muscle tissue:– In the walls of hollow organs, e.g., stomach,

urinary bladder, and airways– Not striated– Involuntary– More details later in this chapter

Figure 9.1

Bone

Perimysium

Endomysium(between individualmuscle fibers)

Muscle fiber

Fascicle(wrapped by perimysium)

Epimysium

Tendon

Epimysium

Muscle fiberin middle ofa fascicle

Blood vessel

Perimysium

Endomysium

Fascicle(a)

(b)

Table 9.1

Table 9.3

Features of a Sarcomere• Thick filaments: run the entire length of an A band• Thin filaments: run the length of the I band and partway

into the A band• Z disc: coin-shaped sheet of proteins that anchors the

thin filaments and connects myofibrils to one another• H zone: lighter midregion where filaments do not

overlap • M line: line of protein myomesin that holds adjacent

thick filaments together

Figure 9.2c, d

I band I bandA bandSarcomere

H zoneThin (actin)filament

Thick (myosin)filament

Z disc Z disc

M line

(c) Small part of one myofibril enlarged to show the myofilamentsresponsible for the banding pattern. Each sarcomere extends fromone Z disc to the next.

Z disc Z discM line

Sarcomere

Thin (actin)filament

Thick(myosin)filament

Elastic (titin)filaments

(d) Enlargement of one sarcomere (sectioned lengthwise). Notice the myosin heads on the thick filaments.

Figure 9.3

Flexible hinge region

Tail

Tropomyosin Troponin Actin

Myosin head

ATP-bindingsite

Heads Active sitesfor myosinattachment

Actinsubunits

Actin-binding sites

Thick filamentEach thick filament consists of manymyosin molecules whose heads protrude at opposite ends of the filament.

Thin filamentA thin filament consists of two strandsof actin subunits twisted into a helix plus two types of regulatory proteins(troponin and tropomyosin).

Thin filamentThick filament

In the center of the sarcomere, the thickfilaments lack myosin heads. Myosin heads are present only in areas of myosin-actin overlap.

Longitudinal section of filamentswithin one sarcomere of a myofibril

Portion of a thick filamentPortion of a thin filament

Myosin molecule Actin subunits

Sarcoplasmic Reticulum (SR)

• Network of smooth endoplasmic reticulum surrounding each myofibril

• Pairs of terminal cisternae form perpendicular cross channels

• Functions in the regulation of intracellular Ca2+ levels

T Tubules

• Continuous with the sarcolemma• Penetrate the cell’s interior at each A band–I

band junction• Associate with the paired terminal cisternae

to form triads that encircle each sarcomere

Triad Relationships

• T tubules conduct impulses deep into muscle fiber

• Integral proteins protrude into the intermembrane space from T tubule and SR cisternae membranes

• T tubule proteins: voltage sensors• SR foot proteins: gated channels that regulate

Ca2+ release from the SR cisternae

Figure 9.5

Myofibril

Myofibrils

Triad:

Tubules ofthe SR

Sarcolemma

Sarcolemma

Mitochondria

I band I bandA band

H zone Z discZ disc

Part of a skeletalmuscle fiber (cell)

• T tubule• Terminal

cisternaeof the SR (2)

M line

Sliding Filament Model of Contraction

• In the relaxed state, thin and thick filaments overlap only slightly

• During contraction, myosin heads bind to actin, detach, and bind again, to propel the thin filaments toward the M line

• As H zones shorten and disappear, sarcomeres shorten, muscle cells shorten, and the whole muscle shortens

Figure 9.6

I

Fully relaxed sarcomere of a muscle fiber

Fully contracted sarcomere of a muscle fiber

IA

Z ZH

I IA

Z Z

1

2

Requirements for Skeletal Muscle Contraction

1. Activation: neural stimulation at aneuromuscular junction

2. Excitation-contraction coupling: – Generation and propagation of an action

potential along the sarcolemma– Final trigger: a brief rise in intracellular Ca2+

levels

Events at the Neuromuscular Junction

• Skeletal muscles are stimulated by somatic motor neurons

• Axons of motor neurons travel from the central nervous system via nerves to skeletal muscles

• Each axon forms several branches as it enters a muscle

• Each axon ending forms a neuromuscular junction with a single muscle fiber

Nucleus

Actionpotential (AP)

Myelinated axonof motor neuron

Axon terminal ofneuromuscular junction

Sarcolemma ofthe muscle fiber

Ca2+Ca2+

Axon terminalof motor neuron

Synaptic vesiclecontaining ACh

MitochondrionSynapticcleft

Fusing synaptic vesicles

1 Action potential arrives ataxon terminal of motor neuron.

2 Voltage-gated Ca2+ channels open and Ca2+ enters the axon terminal.

Figure 9.8

Neuromuscular Junction

• Situated midway along the length of a muscle fiber

• Axon terminal and muscle fiber are separated by a gel-filled space called the synaptic cleft

• Synaptic vesicles of axon terminal contain the neurotransmitter acetylcholine (ACh)

• Junctional folds of the sarcolemma contain ACh receptors

Events at the Neuromuscular Junction

• Nerve impulse arrives at axon terminal• ACh is released and binds with receptors on

the sarcolemma• Electrical events lead to the generation of an

action potential

Figure 9.8

Nucleus

Actionpotential (AP)

Myelinated axonof motor neuron

Axon terminal ofneuromuscular junction

Sarcolemma ofthe muscle fiber

Ca2+Ca2+


Synaptic vesiclecontaining AChMitochondrionSynapticcleft

Junctionalfolds ofsarcolemma

Fusing synaptic vesicles

ACh

Sarcoplasm ofmuscle fiber

Postsynaptic membraneion channel opens;ions pass.

Na+ K+

Ach–

Na+

K+

Degraded ACh

Acetyl-cholinesterase

Postsynaptic membraneion channel closed;ions cannot pass.

1 Action potential arrives ataxon terminal of motor neuron.

2 Voltage-gated Ca2+ channels open and Ca2+ enters the axon terminal.

3 Ca2+ entry causes some synaptic vesicles to release their contents (acetylcholine)by exocytosis.

4 Acetylcholine, aneurotransmitter, diffuses across the synaptic cleft and binds to receptors in the sarcolemma.

5 ACh binding opens ionchannels that allow simultaneous passage of Na+ into the musclefiber and K+ out of the muscle fiber.

6 ACh effects are terminated by its enzymatic breakdown in the synaptic cleft by acetylcholinesterase.

Events in Generation of an Action Potential

1. Local depolarization (end plate potential):– ACh binding opens chemically (ligand) gated ion

channels– Simultaneous diffusion of Na+ (inward) and K+

(outward)– More Na+ diffuses, so the interior of the

sarcolemma becomes less negative– Local depolarization – end plate potential


2. Generation and propagation of an action potential:

– End plate potential spreads to adjacent membrane areas

– Voltage-gated Na+ channels open– Na+ influx decreases the membrane voltage

toward a critical threshold– If threshold is reached, an action potential is

generated


• Local depolarization wave continues to spread, changing the permeability of the sarcolemma

• Voltage-regulated Na+ channels open in the adjacent patch, causing it to depolarize to threshold


3. Repolarization:• Na+ channels close and voltage-gated K+

channels open• K+ efflux rapidly restores the resting polarity• Fiber cannot be stimulated and is in a

refractory period until repolarization is complete

• Ionic conditions of the resting state are restored by the Na+-K+ pump


1. Local depolarization (end plate potential):– ACh binding opens chemically (ligand) gated ion

channels– Simultaneous diffusion of Na+ (inward) and K+

(outward)– More Na+ diffuses, so the interior of the

sarcolemma becomes less negative– Local depolarization – end plate potential


2. Generation and propagation of an action potential:

– End plate potential spreads to adjacent membrane areas

– Voltage-gated Na+ channels open– Na+ influx decreases the membrane voltage

toward a critical threshold– If threshold is reached, an action potential is

generated


• Local depolarization wave continues to spread, changing the permeability of the sarcolemma

• Voltage-regulated Na+ channels open in the adjacent patch, causing it to depolarize to threshold


3. Repolarization:• Na+ channels close and voltage-gated K+

channels open• K+ efflux rapidly restores the resting polarity• Fiber cannot be stimulated and is in a

refractory period until repolarization is complete

• Ionic conditions of the resting state are restored by the Na+-K+ pump

Figure 9.9

Na+

Na+

Open Na+

Channel

Closed Na+

Channel

Closed K+

Channel

Open K+

Channel

Action potential++++++

+++++

+

Axon terminal

Synapticcleft

ACh

ACh

Sarcoplasm of muscle fiber

K+

2 Generation and propagation ofthe action potential (AP)

3 Repolarization

1 Local depolarization: generation of the end plate potential on the sarcolemma

K+

K+Na+

K+Na+

Wave ofde

po

lari

zatio

n

Figure 9.9, step 1

Na+

Na+

Open Na+

ChannelClosed K+

Channel

K+

Na+ K+Action potential

++++++

+++++

+

Axon terminal

Synapticcleft

ACh

ACh


K+


1

Wave ofde

po

lari

zatio

n

Figure 9.9, step 2

Na+

Na+

Open Na+

ChannelClosed K+

Channel

K+

Na+ K+Action potential

++++++

+++++

+

Axon terminal

Synapticcleft

ACh

ACh


K+

Generation and propagation of the action potential (AP)


2

1

Wave ofde

po

lari

zatio

n

Figure 9.9, step 3

Na+

Closed Na+

ChannelOpen K+

Channel

K+

Repolarization3

Figure 9.9

Na+

Na+

Open Na+

ChannelClosed K+

Channel

Action potential++++++

+++++

+

Axon terminal

Synapticcleft

ACh

ACh


K+

2 Generation and propagation ofthe action potential (AP)

3 Repolarization


K+

K+Na+

K+Na+

Wave ofde

po

lari

zatio

n

Closed Na+

ChannelOpen K+

Channel

Figure 9.10

Na+ channelsclose, K+ channelsopen

K+ channelsclose

Repolarizationdue to K+ exit

Threshold

Na+

channelsopen

Depolarizationdue to Na+ entry

Excitation-Contraction (E-C) Coupling

• Sequence of events by which transmission of an AP along the sarcolemma leads to sliding of the myofilaments

• Latent period:– Time when E-C coupling events occur– Time between AP initiation and the beginning of

contraction

Events of Excitation-Contraction (E-C) Coupling

• AP is propagated along sarcomere to T tubules• Voltage-sensitive proteins stimulate Ca2+

release from SR – Ca2+ is necessary for contraction

Figure 9.11, step 1


Muscle fiberTriad

One sarcomere

Synaptic cleft

Setting the stage

Sarcolemma

Action potentialis generated

Terminal cisterna of SR ACh

Ca2+

Figure 9.11, step 2

Action potential is propagated alongthe sarcolemma and down the T tubules.

Steps in E-C Coupling:

Troponin Tropomyosinblocking active sites

Myosin

Actin

Active sites exposed and ready for myosin binding

Ca2+

Terminal cisterna of SR

Voltage-sensitivetubule protein

T tubule

Ca2+

releasechannel

Myosincross bridge

Ca2+

Sarcolemma

Calcium ions are released.

Calcium binds to troponin andremoves the blocking action oftropomyosin.

Contraction begins

The aftermath

1

2

3

4

Figure 9.11, step 3

Steps inE-C Coupling:



T tubule

Ca2+

releasechannel

Ca2+

Sarcolemma

Action potential ispropagated along thesarcolemma and downthe T tubules.

1

Figure 9.11, step 4

Steps inE-C Coupling:



T tubule

Ca2+

releasechannel

Ca2+

Sarcolemma

Action potential ispropagated along thesarcolemma and downthe T tubules.

Calciumions arereleased.

1

2

Figure 9.11, step 5

Troponin Tropomyosinblocking active sitesMyosin

Actin

Ca2+

The aftermath

Figure 9.11, step 6


Actin


Ca2+

Calcium binds totroponin and removesthe blocking action oftropomyosin.

The aftermath

3

Figure 9.11, step 7


Actin


Ca2+

Myosincross bridge

Calcium binds totroponin and removesthe blocking action oftropomyosin.

Contraction begins

The aftermath

3

4

Figure 9.11, step 8

Action potential is propagated alongthe sarcolemma and down the T tubules.

Steps in E-C Coupling:

Troponin Tropomyosinblocking active sites

Myosin

Actin


Ca2+



T tubule

Ca2+

releasechannel

Myosincross bridge

Ca2+

Sarcolemma

Calcium ions are released.

Calcium binds to troponin andremoves the blocking action oftropomyosin.

Contraction begins

The aftermath

1

2

3

4

Role of Calcium (Ca2+) in Contraction

• At low intracellular Ca2+ concentration:– Tropomyosin blocks the active sites on actin– Myosin heads cannot attach to actin– Muscle fiber relaxes

Role of Calcium (Ca2+) in Contraction

• At higher intracellular Ca2+ concentrations:– Ca2+ binds to troponin – Troponin changes shape and moves tropomyosin

away from active sites– Events of the cross bridge cycle occur – When nervous stimulation ceases, Ca2+ is pumped

back into the SR and contraction ends

Cross Bridge Cycle

• Continues as long as the Ca2+ signal and adequate ATP are present

• Cross bridge formation—high-energy myosin head attaches to thin filament

• Working (power) stroke—myosin head pivots and pulls thin filament toward M line

Cross Bridge Cycle

• Cross bridge detachment—ATP attaches to myosin head and the cross bridge detaches

• “Cocking” of the myosin head—energy from hydrolysis of ATP cocks the myosin head into the high-energy state

Figure 9.12

1

Actin

Cross bridge formation.

Cocking of myosin head. The power (working) stroke.

Cross bridge detachment.

Ca2+

Myosincross bridge

Thick filament

Thin filament

ADP

Myosin

Pi

ATPhydrolysis

ATP

ATP

24

3

ADP

Pi

ADPPi

Motor Unit: The Nerve-Muscle Functional Unit

• Motor unit = a motor neuron and all (four to several hundred) muscle fibers it supplies

Figure 9.13a

Spinal cord

Motor neuroncell body

Muscle

Nerve

Motorunit 1

Motorunit 2

Musclefibers

Motorneuronaxon

Axon terminals atneuromuscular junctions

Axons of motor neurons extend from the spinal cord to the muscle. There each axon divides into a number of axon terminals that form neuromuscular junctions with muscle fibers scattered throughout the muscle.

Response to Change in Stimulus Strength

• Threshold stimulus: stimulus strength at which the first observable muscle contraction occurs

• Muscle contracts more vigorously as stimulus strength is increased above threshold

• Contraction force is precisely controlled by recruitment (multiple motor unit summation), which brings more and more muscle fibers into action

Figure 9.16

Stimulus strength

Proportion of motor units excited

Strength of muscle contraction

Maximal contraction

Maximalstimulus

Thresholdstimulus

Response to Change in Stimulus Strength

• Size principle: motor units with larger and larger fibers are recruited as stimulus intensity increases

Muscle Tone

• Constant, slightly contracted state of all muscles

• Due to spinal reflexes that activate groups of motor units alternately in response to input from stretch receptors in muscles

• Keeps muscles firm, healthy, and ready to respond

Muscle Metabolism: Energy for Contraction

• ATP is regenerated by:– Direct phosphorylation of ADP by creatine

phosphate (CP) – Anaerobic pathway (glycolysis) – Aerobic respiration

Figure 9.19a

Coupled reaction of creatinephosphate (CP) and ADP

Energy source: CP

(a) Direct phosphorylation

Oxygen use: NoneProducts: 1 ATP per CP, creatineDuration of energy provision:15 seconds

Creatinekinase

ADPCP

Creatine ATP

Figure 9.19b

Energy source: glucose

Glycolysis and lactic acid formation

(b) Anaerobic pathway

Oxygen use: NoneProducts: 2 ATP per glucose, lactic acidDuration of energy provision:60 seconds, or slightly more

Glucose (fromglycogen breakdown ordelivered from blood)

Glycolysisin cytosol

Pyruvic acid

Releasedto blood

net gain

2

Lactic acid

O2

O2ATP

Figure 9.19c

Energy source: glucose; pyruvic acid;free fatty acids from adipose tissue;amino acids from protein catabolism

(c) Aerobic pathway

Aerobic cellular respiration

Oxygen use: RequiredProducts: 32 ATP per glucose, CO2, H2ODuration of energy provision: Hours

Glucose (fromglycogen breakdown ordelivered from blood)

32

O2

O2

H2O

CO2

Pyruvic acidFattyacids

Aminoacids

Aerobic respirationin mitochondriaAerobic respirationin mitochondria

ATP

net gain perglucose

Oxygen Deficit

Extra O2 needed after exercise for:

• Replenishment of– Oxygen reserves – Glycogen stores – ATP and CP reserves

• Conversion of lactic acid to pyruvic acid, glucose, and glycogen

Heat Production During Muscle Activity

• ~ 40% of the energy released in muscle activity is useful as work

• Remaining energy (60%) given off as heat • Dangerous heat levels are prevented by

radiation of heat from the skin and sweating

Force of Muscle Contraction

• The force of contraction is affected by:– Number of muscle fibers stimulated (recruitment)– Relative size of the fibers—hypertrophy of cells

increases strength

Velocity and Duration of Contraction

Influenced by:1. Muscle fiber type2. Load3. Recruitment

Muscle Fiber Type

Classified according to two characteristics:1. Speed of contraction: slow or fast, according

to:– Speed at which myosin ATPases split ATP– Pattern of electrical activity of the motor neurons

Muscle Fiber Type

2. Metabolic pathways for ATP synthesis:– Oxidative fibers—use aerobic pathways– Glycolytic fibers—use anaerobic glycolysis

Muscle Fiber Type

Three types: – Slow oxidative fibers– Fast oxidative fibers– Fast glycolytic fibers

Table 9.2

Effects of Resistance Exercise

• Resistance exercise (typically anaerobic) results in:– Muscle hypertrophy (due to increase in fiber size)– Increased mitochondria, myofilaments, glycogen

stores, and connective tissue

Smooth Muscle

• Found in walls of most hollow organs(except heart)

• Usually in two layers (longitudinal and circular)

Peristalsis

• Alternating contractions and relaxations of smooth muscle layers that mix and squeeze substances through the lumen of hollow organs– Longitudinal layer contracts; organ dilates and

shortens – Circular layer contracts; organ constricts and

elongates

Microscopic Structure

• Spindle-shaped fibers: thin and short compared with skeletal muscle fibers

• Connective tissue: endomysium only• SR: less developed than in skeletal muscle • Pouchlike infoldings (caveolae) of sarcolemma

sequester Ca2+

• No sarcomeres, myofibrils, or T tubules

Myofilaments in Smooth Muscle

• Ratio of thick to thin filaments (1:13) is much lower than in skeletal muscle (1:2)

• Thick filaments have heads along their entire length

• No troponin complex; protein calmodulin binds Ca2+

Role of Calcium Ions

• Ca2+ binds to and activates calmodulin • Activated calmodulin activates myosin (light

chain) kinase• Activated kinase phosphorylates and activates

myosin • Cross bridges interact with actin

Special Features of Smooth Muscle Contraction

Hyperplasia:– Smooth muscle cells can divide and increase their

numbers– Example:

• estrogen effects on uterus at puberty and during pregnancy

Functions of the Nervous System

1. Sensory input– Information gathered by sensory receptors about

internal and external changes

2. Integration– Interpretation of sensory input

3. Motor output– Activation of effector organs (muscles and

glands) produces a response

Peripheral Nervous System (PNS)

• Two functional divisions1. Sensory (afferent) division

• Somatic afferent fibers — convey impulses from skin, skeletal muscles, and joints

• Visceral afferent fibers — convey impulses from visceral organs

2. Motor (efferent) division • Transmits impulses from the CNS to effector organs

Motor Division of PNS

1. Somatic (voluntary) nervous system– Conscious control of skeletal muscles

Motor Division of PNS

2. Autonomic (involuntary) nervous system (ANS); “ a law unto itself”

– Visceral motor nerve fibers– Regulates smooth muscle, cardiac muscle, and

glands– Two functional subdivisions

• Sympathetic• Parasympathetic

Histology of Nervous Tissue

• Two principal cell types1. Neurons — excitable cells that transmit electrical

signals

Histology of Nervous Tissue

2. Neuroglia (glial cells)—supporting cells:• Astrocytes (CNS)• Microglia (CNS)• Ependymal cells (CNS)• Oligodendrocytes (CNS)• Satellite cells (PNS)• Schwann cells (PNS)

Astrocytes

• Most abundant, versatile, and highly branched glial cells

• Cling to neurons, synaptic endings, and capillaries

• Support and brace neurons

Astrocytes

• Help determine capillary permeability• Guide migration of young neurons• Control the chemical environment• Participate in information processing in the

brain

Microglia

• Small, ovoid cells with thorny processes• Migrate toward injured neurons• Phagocytize microorganisms and neuronal

debris

Ependymal Cells

• Range in shape from squamous to columnar• May be ciliated

– Line the central cavities of the brain (ventricles) and spinal column

– Separate the CNS interstitial fluid from the cerebrospinal fluid in the cavities

– Circulates CSF

Oligodendrocytes

• Branched cells• Processes wrap CNS nerve fibers, forming

insulating myelin sheaths

Satellite Cells and Schwann Cells

• Satellite cells– Surround neuron cell bodies in the PNS

• Schwann cells (neurolemmocytes)– Surround peripheral nerve fibers and form myelin

sheaths– Vital to regeneration of damaged peripheral

nerve fibers

Neurons (Nerve Cells)

• Special characteristics:– Long-lived ( 100 years or more)– Amitotic—with few exceptions– High metabolic rate—depends on continuous

supply of oxygen and glucose– Plasma membrane functions in:

• Electrical signaling • Cell-to-cell interactions during development

Cell Body (Perikaryon or Soma)

• Biosynthetic center of a neuron• Spherical nucleus with nucleolus• Well-developed Golgi apparatus• Rough ER called Nissl bodies (chromatophilic

substance)

Cell Body (Perikaryon or Soma)

• Network of neurofibrils (neurofilaments) • Axon hillock — cone-shaped area from which

axon arises• Clusters of cell bodies are called nuclei in the

CNS, ganglia in the PNS

Processes

• Dendrites and axons• Bundles of processes are called

– Tracts in the CNS– Nerves in the PNS

Dendrites

• Short, tapering, and diffusely branched • Receptive (input) region of a neuron• Convey electrical signals toward the cell body

as graded potentials

The Axon• One axon per cell arising from the axon

hillock• Long axons (nerve fibers)• Occasional branches (axon collaterals)

The Axon

• Numerous terminal branches (telodendria)• Knoblike axon terminals (synaptic knobs or

boutons) – Secretory region of neuron– Release neurotransmitters to excite or inhibit

other cells

Axons: Function

• Conducting region of a neuron• Generates and transmits nerve impulses

(action potentials) away from the cell body

Myelin Sheath

• Segmented protein-lipoid sheath around most long or large-diameter axons

• It functions to:– Protect and electrically insulate the axon– Increase speed of nerve impulse transmission

Myelin Sheaths in the PNS

• Schwann cells wraps many times around the axon – Myelin sheath — concentric layers of Schwann

cell membrane

• Neurilemma — peripheral bulge of Schwann cell cytoplasm

Myelin Sheaths in the PNS

• Nodes of Ranvier – Myelin sheath gaps between adjacent Schwann

cells– Sites where axon collaterals can emerge

Myelin Sheaths in the CNS

• Formed by processes of oligodendrocytes, not the whole cells

• Nodes of Ranvier are present• No neurilemma• Thinnest fibers are unmyelinated

Functional Classification of Neurons

• Three types: 1. Sensory (afferent)

• Transmit impulses from sensory receptors toward the CNS

2. Motor (efferent)• Carry impulses from the CNS to effectors

Functional Classification of Neurons

3. Interneurons (association neurons)• Shuttle signals through CNS pathways; most are

entirely within the CNS

Neuron Function

• Neurons are highly irritable• Respond to adequate stimulus by generating

an action potential (nerve impulse) • Impulse is always the same regardless of

stimulus

Role of Membrane Ion Channels

• Proteins serve as membrane ion channels• Two main types of ion channels

1. Leakage (nongated) channels—always open

Role of Membrane Ion Channels

2. Gated channels (three types):– Chemically gated (ligand-gated) channels—open with binding

of a specific neurotransmitter– Voltage-gated channels—open and close in response to

changes in membrane potential– Mechanically gated channels—open and close in response to

physical deformation of receptors

Gated Channels

• When gated channels are open:– Ions diffuse quickly across the membrane along

their electrochemical gradients• Along chemical concentration gradients from higher

concentration to lower concentration• Along electrical gradients toward opposite electrical

charge– Ion flow creates an electrical current and voltage

changes across the membrane

Resting Membrane Potential (Vr)

• Potential difference across the membrane of a resting cell– Approximately –70 mV in neurons (cytoplasmic

side of membrane is negatively charged relative to outside)

• Generated by:– Differences in ionic makeup of ICF and ECF – Differential permeability of the plasma membrane

Resting Membrane Potential

• Differences in ionic makeup– ICF has lower concentration of Na+ and Cl– than

ECF– ICF has higher concentration of K+ and negatively

charged proteins (A–) than ECF


• Differential permeability of membrane– Impermeable to A–

– Slightly permeable to Na+ (through leakage channels)

– 75 times more permeable to K+ (more leakage channels)

– Freely permeable to Cl–


• Negative interior of the cell is due to much greater diffusion of K+ out of the cell than Na+ diffusion into the cell

• Sodium-potassium pump stabilizes the resting membrane potential by maintaining the concentration gradients for Na+ and K+

Membrane Potentials That Act as Signals

• Two types of signals– Graded potentials

• Incoming short-distance signals

– Action potentials • Long-distance signals of axons

Changes in Membrane Potential

• Depolarization– A reduction in membrane potential (toward zero)– Inside of the membrane becomes less negative

than the resting potential– Increases the probability of producing a nerve

impulse

Figure 11.9a

Depolarizing stimulus

Time (ms)

Insidepositive

Insidenegative

Restingpotential

Depolarization

(a) Depolarization: The membrane potentialmoves toward 0 mV, the inside becoming less negative (more positive).

Changes in Membrane Potential

• Hyperpolarization– An increase in membrane potential (away from

zero)– Inside of the membrane becomes more negative

than the resting potential– Reduces the probability of producing a nerve

impulse

Figure 11.9b

Hyperpolarizing stimulus

Time (ms)

Restingpotential

Hyper-polarization

(b) Hyperpolarization: The membranepotential increases, the inside becomingmore negative.

Graded Potentials

• Short-lived, localized changes in membrane potential

• Depolarizations or hyperpolarizations• Graded potential spreads as local currents

change the membrane potential of adjacent regions

Figure 11.10b

(b) Spread of depolarization: The local currents (black arrows) that are created depolarize adjacent membrane areas and allow the wave of depolarization to spread.

Graded Potentials

• Occur when a stimulus causes gated ion channels to open– E.g., receptor potentials, generator potentials,

postsynaptic potentials (IPSP, EPSP)• Magnitude varies directly (graded) with

stimulus strength • Decrease in magnitude with distance as ions

flow and diffuse through leakage channels• Short-distance signals

Action Potential (AP)

• Brief reversal of membrane potential with a total amplitude of ~100 mV

• Occurs in muscle cells and axons of neurons• Does not decrease in magnitude over

distance• Principal means of long-distance neural

communication

Actionpotential

1 2 3

4

Resting state Depolarization Repolarization

Hyperpolarization

The big picture

1 1

2

3

4

Time (ms)

ThresholdMem

bra

ne p

ote

nti

al (m

V)

Figure 11.11 (1 of 5)

Generation of an Action Potential

• Resting state– Only leakage channels for Na+ and K+ are open– All gated Na+ and K+ channels are closed

Depolarizing Phase

• Depolarizing local currents open voltage-gated Na+ channels

• Na+ influx causes more depolarization• At threshold (–55 to –50 mV) positive

feedback leads to opening of all Na+ channels, and a reversal of membrane polarity to +30mV (spike of action potential)

Repolarizing Phase

• Repolarizing phase– Na+ channel slow inactivation gates close– Membrane permeability to Na+ declines to

resting levels– Slow voltage-sensitive K+ gates open– K+ exits the cell and internal negativity is restored

Hyperpolarization

• Hyperpolarization– Some K+ channels remain open, allowing excessive

K+ efflux – This causes hyperpolarization of the membrane

(undershoot)

Propagation of an Action Potential

• Na+ influx causes a patch of the axonal membrane to depolarize

• Local currents occur• Na+ channels toward the point of origin are

inactivated and not affected by the local currents

Propagation of an Action Potential

• Local currents affect adjacent areas in the forward direction

• Depolarization opens voltage-gated channels and triggers an AP

• Repolarization wave follows the depolarization wave

• (Fig. 11.12 shows the propagation process in unmyelinated axons.)

Threshold

• At threshold:– Membrane is depolarized by 15 to 20 mV – Na+ permeability increases– Na influx exceeds K+ efflux– The positive feedback cycle begins

Threshold

• Subthreshold stimulus—weak local depolarization that does not reach threshold

• Threshold stimulus—strong enough to push the membrane potential toward and beyond threshold

• AP is an all-or-none phenomenon — action potentials either happen completely, or not at all

Coding for Stimulus Intensity

• All action potentials are alike and are independent of stimulus intensity– How does the CNS tell the difference between a

weak stimulus and a strong one?

• Strong stimuli can generate action potentials more often than weaker stimuli

• The CNS determines stimulus intensity by the frequency of impulses

Figure 11.13

Threshold

Actionpotentials

Stimulus

Time (ms)

Figure 11.14

Stimulus

Absolute refractoryperiod

Relative refractoryperiod

Time (ms)

Depolarization(Na+ enters)

Repolarization(K+ leaves)

After-hyperpolarization

Conduction Velocity

• Conduction velocities of neurons vary widely • Effect of axon diameter

– Larger diameter fibers have less resistance to local current flow and have faster impulse conduction

• Effect of myelination– Continuous conduction in unmyelinated axons is

slower than saltatory conduction in myelinated axons

Conduction Velocity

• Effects of myelination– Myelin sheaths insulate and prevent leakage of

charge– Saltatory conduction in myelinated axons is about

30 times faster• Voltage-gated Na+ channels are located at the nodes• APs appear to jump rapidly from node to node

Electrical Synapses

• Less common than chemical synapses– Neurons are electrically coupled (joined by gap

junctions)– Communication is very rapid, and may be

unidirectional or bidirectional– Are important in:

• Embryonic nervous tissue• Some brain regions

Chemical Synapses

• Specialized for the release and reception of neurotransmitters

• Typically composed of two parts – Axon terminal of the presynaptic neuron, which

contains synaptic vesicles – Receptor region on the postsynaptic neuron

Synaptic Cleft

• Fluid-filled space separating the presynaptic and postsynaptic neurons

• Prevents nerve impulses from directly passing from one neuron to the next

Synaptic Cleft

• Transmission across the synaptic cleft: – Is a chemical event (as opposed to an electrical

one)– Involves release, diffusion, and binding of

neurotransmitters– Ensures unidirectional communication between

neurons

Information Transfer

• AP arrives at axon terminal of the presynaptic neuron and opens voltage-gated Ca2+ channels

• Synaptotagmin protein binds Ca2+ and promotes fusion of synaptic vesicles with axon membrane

• Exocytosis of neurotransmitter occurs

Information Transfer

• Neurotransmitter diffuses and binds to receptors (often chemically gated ion channels) on the postsynaptic neuron

• Ion channels are opened, causing an excitatory or inhibitory event (graded potential)

Figure 11.17

Action potentialarrives at axon terminal.

Voltage-gated Ca2+

channels open and Ca2+

enters the axon terminal.

Ca2+ entry causesneurotransmitter-containing synapticvesicles to release theircontents by exocytosis.

Chemical synapsestransmit signals fromone neuron to anotherusing neurotransmitters.

Ca2+

Synapticvesicles

Axonterminal

Mitochondrion

Postsynapticneuron

Presynapticneuron

Presynapticneuron

Synapticcleft

Ca2+

Ca2+

Ca2+

Neurotransmitterdiffuses across the synapticcleft and binds to specificreceptors on thepostsynaptic membrane.

Binding of neurotransmitteropens ion channels, resulting ingraded potentials.

Neurotransmitter effects areterminated by reuptake throughtransport proteins, enzymaticdegradation, or diffusion awayfrom the synapse.

Ion movement

Graded potentialReuptake

Enzymaticdegradation

Diffusion awayfrom synapse

Postsynapticneuron

1

2

3

4

5

6

Postsynaptic Potentials

• Graded potentials• Strength determined by:

– Amount of neurotransmitter released– Time the neurotransmitter is in the area

• Types of postsynaptic potentials 1. EPSP—excitatory postsynaptic potentials 2. IPSP—inhibitory postsynaptic potentials

Table 11.2 (1 of 4)

Table 11.2 (2 of 4)

Table 11.2 (3 of 4)

Table 11.2 (4 of 4)

Excitatory Synapses and EPSPs

• Neurotransmitter binds to and opens chemically gated channels that allow simultaneous flow of Na+ and K+ in opposite directions

• Na+ influx is greater that K+ efflux, causing a net depolarization

• EPSP helps trigger AP at axon hillock if EPSP is of threshold strength and opens the voltage-gated channels

Figure 11.18a

An EPSP is a localdepolarization of the postsynaptic membranethat brings the neuroncloser to AP threshold. Neurotransmitter binding opens chemically gated ion channels, allowing the simultaneous pas-sage of Na+ and K+.

Time (ms)

(a) Excitatory postsynaptic potential (EPSP)

Threshold

Stimulus

Mem

bra

ne p

ote

nti

al (m

V)

Inhibitory Synapses and IPSPs

• Neurotransmitter binds to and opens channels for K+ or Cl–

• Causes a hyperpolarization (the inner surface of membrane becomes more negative)

• Reduces the postsynaptic neuron’s ability to produce an action potential

Figure 11.18b

An IPSP is a localhyperpolarization of the postsynaptic membraneand drives the neuron away from AP threshold. Neurotransmitter binding opens K+ or Cl– channels.

Time (ms)

(b) Inhibitory postsynaptic potential (IPSP)

Threshold

Stimulus

Mem

bra

ne p

ote

nti

al (m

V)

Integration: Summation

• A single EPSP cannot induce an action potential

• EPSPs can summate to reach threshold• IPSPs can also summate with EPSPs, canceling

each other out

Integration: Summation

• Temporal summation– One or more presynaptic neurons transmit

impulses in rapid-fire order

• Spatial summation– Postsynaptic neuron is stimulated by a large

number of terminals at the same time

Figure 11.23

1

2

3

4

5

Receptor

Sensory neuron

Integration center

Motor neuron

Effector

Stimulus

ResponseSpinal cord (CNS)

Interneuron

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