Bio Notes 2
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7.1 Getting Moving
Muscles contract + relax
to bend (flex) and straighten (extend)
eg. Ankles, knees, hip joints
Joints & Movement
- Muscles bring movement at joint
- Muscles shorten, pulling bone, moving joint
- Muscles only pull so work in antagonistic pairs
- Muscles for extension of joint = Extensor
Flexor= bends joint
Joint Structure
Hip, knee, ankle = Synovial joints
Bones separated by cavity of synovial fluid
Held in position by ligaments
Cartilage protects
Muscles
How do they work?
- Bundles of muscle fibres. Multinucleate as
single nucleus couldnt control metabolism of
such long cell.
- Prenatal dev, several cells fuse together to
form long fibre.
- Muscle made up of bundles of muscle fibres.
Bound by connective tissue.
- Bundle made up of single muscle fibres
- Muscle fibre made up of myofibrils
- Myofibril made up of sarcomeres contractile
Light band= Actin. Dark band= Myosin+Actin .
Medium= Myosin.
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How Sarcomere shortens
- Sliding Filament Theory-
- Nerve impulse arrives at neuromuscular
junction.
- Ca ions released from sarcoplasmic reticulum.Diffuse through
sarcoplasm
- Ca attaches to troponin molecule.
- Tropomyosin shifts, exposing binding sites.
- Myosin heads bind with sites, forming cross
bridges.
-ADP + Pi released from head
- Myosin changes shape + head nods forward,
-
- So head returns to upright position.
Many myosin heads nodding = many
movements of actin, causing muscle contraction.
When muscle relaxes, not stim by nerve
impulses, and Ca
pumped out of sarcoplasm using ATP.
Troponin and myosin move back.
7.2 Energy for Action
BMR = min energy requirement at rest to fuel
basic
metabolic processes. Prop. to body SA.
Releasing EnergyCarbs + fats.
Enzyme controlled reactions = respiration,
synthesis, ATP.
ATP created from ADP + Pi.
- In solution, phosphate ions are hydrated.
- To make ATP, must be separated from water.
- ATP in water higher energy than ADP + Pi in
water.
-
ATP in water ADP + hydrated Pi + energy
Carb Oxidation
C6H12O6 + 6O2 6CO2 + 6H2O + energy
- In aerobic resp, H in glucose bonds with O toform water
again. Energy release , to generate ATP.
- Glucose + oxygen not brought together directly
as too much energy too quickly. So, glycolysis.
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Glycolysis
* Stores of glycogen in muscle/liver converted to
glucose.
* Adding phosphate to glucose = ^ reactivity.
* Glucose is at higher energy level than
pyruvate, so energy becomes available.
Phosphate from intermediate compounds
transferred to
ADP > ATP.
= substrate level phosphorylation. because energyfor ATP comes
fr
om substrates
So, two ATPs, 2 pairs of H, 2 molecules of
pyruvate produced.
Fate of Pyruvate- Aerobic
- Pyruvate passed into mitochondria. Oxidised.
Link Reaction
- Decarboxylated (CO2 released0029- Dehydrogenated (2 hydrogens removed +
taken up by
coenzyme
NAD )
Resulting 2C combines with CoA > Acetyl CoA
Carries to Krebs cycle
Producing 2 CO2, 1 ATP, 4 pairs of H (reducing
NAD + FAD)
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Fate of the Hydrogens- Electron Transport
- Reduced NAD and FAD shuttle H atoms to
electron chain on mitochondrial inner
membrane.
- The H electrons and protons separate.
* Reduced NAD becomes NAD.
* Electrons passed along carriers in redox
reactions.
* Protons move across inner m. membrane,
creating ^ conc.
in intermembrane space, then diffuse back
down
electrochem grad.
ATP synthesis by chemiosmosis
- Energy is released as the electrons are passed
down.
- Energy moves hydrogen ions to intermembrane
space,
= electrochem gradient across inner m.
membrane,
so intermembrane space more pos.
* H diffuse down through hollow proteinchannels.
* ATP synthesis catalysed.
* H cause conformational change in the ATPase
active site,
How much ATP Produced?
- Varies according to efficiency of cell
- Roughly max. of 38 per glucose,
as each rNAD 3 ATP, each rFAD 2 ATP
- Actual yield around 30 as the electrochem gradused for
other ion transport.
Rate of Respiration
- Measure using respirometer
- Affected by enzyme conc, substrate conc,
temp, pH.
- As living orgs in exp. tube take up oxygen, fluid
- Potassium hydroxide (KOH) solution in other
tube absorbs
CO2, compensating for change in vol. due to
variation in
gas pressure of temp. inside apparatus.
- Conc. of ATP also controls resp rate. Inhibs
enzyme in first step of glycolysis,
phosphorylation of glucose:
- In presence of ATP, shape of enzyme
inactive.
As ATP broken down active.
= oint inhib. End roduct inhibs earlier
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Fate of pyruvate- Anaerobic
- Electron chain ceases as rNAD, link reaction,
and krebs cycle arent oxidised.
- Can oxidise rNAD (from glycolysis) without O.
- Reduced pyruvate Lactate + oxidised NAD
- So still partially break down glucose to make
small amount of ATP (2 ATP per glucose)
- Lactate must be disposed of as it forms lactic
acid solution,reducing pH, inhib enzymes, so glycolysis cant
cont.
Effect of Lactate Build Up
Aminos in enzymes pos or neg charge groups.
H ions from lactic acid accumulate in cytoplasm,
neutralise neg groups in enzyme active site.
So substrate cant bind.
Getting Rid of Lactate
- Most lactate converted back to pyruvate that is
oxidised to CO2 and water via krebs for ATP.
- Result is O uptake is greater than normal in
recovery period= Oxygen debt . post-exercise O consumption
- Some lactate converted to glycogen for
muscles + liver.
Supplying Instant Energy
- At the start of exercise, ATP regenerated using
creatine phosphate,
stored in muscles + hydrolysed to release
energy.
Used to make ATP from ADP+Pi (Pi from
creatine)
-Formation of ADP triggers breakdown
breakdown of creatine phosphate creatine +
Pi
ADP + Pi = ATP
Reactions dont require O.
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Three Energy Systems
At start of exercise, resp not efficient enough;
not delivering O quick enough.
* First, ATP/PC system + anaerobic resp allow
ATP regen.
* In endurance exercise, ^ blood supply ^ O
supply,
and aerobic resp can regen ATP as quickly as
its broken down.
So sustained exercise poss.
O deficit is diff between actual O
7.3 Peak Performance
Aerobic capacity Ability to take in, transport
and use O.
VO2 = Vol O consumed per min.
VO2 max = Max vol O consumed per min.
Depends on efficiency of uptake +
delivery of O by
lungs + CV systems, and efficient use
by muscle
fibres.
Cardiac output = Vol. blood pumped per min
When running, O supply maintained by:
^ cardiac out ut ^ breathin rate dee er
Cardiac Output
- ^ during exercise.
- Depends on stroke vol Vol blood ejected left
ventricle
CO = SV x Heart Rate
Stroke Volume
During exercise, more blood returns to heart in
venous return in diastole.
So more blood fills heart from atria and heart
stretched more, so contracts with greater force,
so more blood expelled.
= ^ SV and CO
Usually at rest, ventricles dont empty
Heart Rate
Bpm.
Differences caused by.. size of heart, body size,
genes.
Larger heart = lower Bpm as higher stroke vol
Training leads to lower Bpm.
Control of Heart Rate
How does it beat?
Beats without nervous system input = Myogenic
Depolarisation causes contraction.
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SAN (sinoatrial node) in right atrium
(pacemaker)
Across Atria AVN
(atrioventricular node)
Contract (systole) Delay so atria
finished
contracting and
ventricles
have filled
Purkyne fibres
Large muscle fibres that
conduct
Measuring electrical activity
Detected + displayed on ECG:
Electrodes on chest + limbs to record currents in
cardiac cycle. Change in polarisation allows
current to be detected.
ECG at rest, or in stress test (before, during,
after exercise)
(to detect heart
problems)
* Heart rate lower 60bpm = Bradycardia
common in athletes but also
symptom of heart problems.
* Heart rate higher 100bpm = Tachycardia
Anxiety, fear, fever, exercise,
CHD.
- Ischaemia = doesnt receive blood as normal
rhythm
disrupted.
- Arrhythmias = Abnormal beat caused by
electrical
disturbance.
Nervous control of heart rate
- CV control central in medulla
- Nerves of ANS lead from CN control centre to
heart
Sympathetic- Accelerate
Stimulated by
Parasympathetic- Decelerate (vagus)
SAN
- CV control centre detects accumulation of CO2
and lactate in blood, lower O and higher temp.
- Mech. activity in muscles + joints detected by
sensory receptors, sending impulse to CN control
centre.
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- When anticipating exercise (fight or flight),
muscles contract, stretch receptors stim, send
impulse,
^ heart rate via sympathetic nerve,
= ^ venous return, ^ stroke volume = ^
cardiac output
= ^ delivered O.
- BP rises with higher cardiac ouput, so receptors
in aorta + carotid artery send impulse to centre
to send to inhib nerve
(to prevent further rise)
* Effect of stim of sympathetic nerve:
^ breathing, ^ heart rate + stroke vol, v
Hormonal effects on heart rate
- Adrenaline from adrenal glands above kidneys
released into bloodstream.
Effects SAN, ^ heart rate (fight/flight)
- Also causes vasodilation of arterioles supplying
skeletal muscles, and constriction of arterioles to
digestive system.
(so more blood flows to active muscles)
BreathingTidal Volume = Vol air breathe in and out in one
breathe.
Vital capacity = Max tidal volume.
Measured with spirometer.
Controlling Breathing
- Ventilation centre in medulla oblongata.
* Inhalation V centre sends impulse to
intercostal +
diaphragm muscles = contract =
inhale.
- If deep, also neck + chest muscles.
* Exhalation Lungs inflate stretch receptors
in
Exhalation caused by elastic recoil of lungs and
gravity lowing ribs. Not all air exhaled.
- Internal intercostals muscles only contract
during deep exhalation, so less residual air.
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Controlling breathing rate + depth
* Concentration of CO2 in blood, due to its effect
on pH.
because..
- CO2 dissolves in blood carbonic acid.
- Acid dissociates into H + H carbonate ions = v
pH in blood
- Chemoreceptors in V centre detect rise.
- Impulses to other parts of V centre.
- Sent to stim muscles.
Frequent deeper breaths maintain conc. gradient
of CO2
between alveolar air + blood efficient removal
Controlling breathing during exercise
- Motor cortex controls movement.
- When exercise starts, impulses from cortex
affect V centre
in medulla, ^ ventilation.
- Also, impulses from stretch receptors in
tendons + muscles.
- Chemoreceptors sensitive to CO2 levels +
blood temp
^ depth + rate of breathing.
All muscle fibres are not the same
Slow Twitch- Dark as a lot of myoglobin.
^ mitochondria, ^ respiratory
enzymes
For slower, sustainedcontraction.
Need aerobic resp.
^ capillaries (for good O supply)
Less glycogen and sarcoplasmic
reticulum.
Fast Twitch- v mitochondria, v myoglobin so v O
+ capillaries
Short burst of energy. Rapid,
Myoglobin = protein similar to haemoglobin.
High affinity for O, acts as O store in
muscle cells.
What makes a sprinter?
- Proportion of each type genetically determined.- ^ Aerobic capacity have ^ proportion of slow
twitch.
- Sprinters v slow switch.
- Throwers + jumpers have equal.
- Inds. better suited to certain type of ex, given
prop.
But other factors eg. efficient CV system well
suited to
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7.4 Breaking out in a Sweat
Homeostasis
To maintain stable, internal env. Optumum.
Partly done by maintaining stable conds in
blood; gives rise to tissue fluid bathing cells.
Conc of glucose, ions, CO2, pH, temp.
Role of Neg Feedback
Norm value / set point.
Receptors detect deviations control mech effectors
Muscles +Glands
To bring back to norm.
Temperature Control
Thermoregulation.
37.5 C allows enzyme controlled reactions
good rate.
Lower too slow, higher denatured
Temp. control receptors and effectors
Temp neg feedback. Receptor detects blood
temp, in hypothalamus. Thermostat
Thermoreceptors in skin send impulse tohypothalamus.
Heat Loss Centre Heat Gain Centre
Stim- Sweat glands Stim- Arterioles constrict
Inhib- -Hair erector
-Contraction of arterioles -Liver ^ metabolic rate
(dilate capillaries) -Skeletal musclescontract
-Hair erector muscles (shiver)
(hairs lie flat) Inhib- Sweat
glands
-Liver (v metabolic rate)
-Skeletal muscles
(no shivering)
-
* Sweat released on skin via sweat ducts
evaporates, taking heat energy from skin.
Sweat glands are stim by nerves from
hypothalamus.
* Erected hairs trap air layer that insulates body.
not as effective as other mammals
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Temp reg during exercise
Core temp rises, related to intensity.
Then neg feedback.
Radiation- We radiate energy as warmer than
env
Conduction- Direct transfer between objects;
energy
transfer
Convection- Air by skin warmed by body, thenreplaced by
colder air, warmed.. (layer of still air
reduces it)
Evaporation- Convert water to vapour. Sweating.
7.5 Overdoing It
Improved nutrition, training, design + materials,
tracks,
has improved performance.
Some athletes overtrain. Burnout symptoms.
Excessive exercise + immune suppression
- Heavy training more prone to infection
Effects of exercise on immunity
Moderate-
^ natural killer cells in blood + lymph.
Unspecific, against cells invaded by viruses and
cancer cells.
- Activated by cytokines + interferons.
- Release perforin (perforate target cell
membranes)
allowing entry of proteases to cause apoptosis
(death)
Vigorous-
During recovery these fall: Nat killers,
phagocytes, B cells,
Also, inflammatory response in damaged muscle
fibres, reducing non-specific (against URT
infection).
Debate- Effects caused by activity or psych
stress.
Both would cause secretion of hormones,
eg. adrenaline, cortisol, which suppress
IS.
How Are Joints Damaged by Exercise?
Force on joints. Wear+tear. Overuse or ageing.
Pain, inflammation, restricted movement.
Treatment: Rest, ice, compression + elevation,
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Knees- Cartilage wears away, bones grind.
Inflam+arthritis.
-Patellor tendonitis. Knee cap doesnt
glide across
femur due to cartilage damage.
- Bursae (fluid sacs) can swell with extra
fluid.
- Sudden twist = damage ligaments.
How can medical technology help?
Keyhole surgery especially for cruciate ligs on knee
Small incisions. Camera + light. Mini
instruments.
-Quick recovery.
Prostheses
Artificial body part for disability.
Now diff designs for diff activities eg. spring foot
Also used to replace damaged/diseased joints.
eg. replacing hips and knees.
For knee, incision, patella moved, then fit in
new surface.
Taking Enough Exercise
Advantages:
^ arterial vasodilation and v BP, v CHD + stroke.
^ blood HDLs and v LDLs (v CHD + arthro)
Healthy weight from balanced energy in to out
^ Bone density + v loss old age, so v
osteoporosis.
v Cancer risk.
^ mental well being.
30 mins, 5 days a week.
Sedentary obesity. BMI 30+ ^bp + LDLs.
CHD + stroke.
7.6 Improving on Nature
Performance Enhancing Substances
Use of drugs to enhance performance = doping
World Anti-Doping Code prohibits substances +
blood doping (extra blood cells) and artificiallyenhancing uptake/transport/delivery of O
(drugs/haemo), gene doping or non-medical use
of cells.
Athletes with medical conds needing prohibited
drugs need permission.
Human growth hormone and testo on list
although natural.
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Hormones
- Chem messengers
- Released into blood from endocrine glands (no
ducts)
- Cells in endocrine ducts have to be unaffected
by the
glands.
- So, hormones produced in inactive form, or
packaged in
vesicles by Golgi.- Vesicles fuse with cell surface membrane,
releasing by
exocytosis.
Gland Hormone FunctionPituitary Growth
Follicle stim
Antidiuretic
Stim growth
Controls
testes +
Ovaries.
Reabsorption
of water in
kidneys.Thyroid Thyroxine ^BMR
Ovary Oestrogen Promote devof
Ovaries +
2ndry
Fem. chars.Testis Testosterone Dev of
* Each hormone affects specific target cells, mod
activity.
* Hormones carried around bloodstream.
* Enter target cells or bind to receptor
molecules.
* Brings response due to effect on enzymes.
* Some bind to receptor producing secondary
messenger that activates enzymes inside cell.
* Others control transcription.
How hormones affect cells
- Peptide hormones are protein chains.
- Small but cant pass through membrane easily
as charged.
Peptide hormones: Insulin, human growth
hormone.
Steroid hormones formed from lipids. Complex
ring structure.
Pass through membrane + bind to receptor
inside cytoplasm. Effects transcription.
The receptor acts as a transcription factor,
switching on/off
enzyme synthesis.
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How Transcription Factors Work
- Initiated by RNA polymerase and assoc
transcription factors binding to DNA.
= Transcription initiation complex.
- Complex binds adjacent to gene being
transcribed.
= promoter region
- Most factors made in inactive form, converted
to active by hormones, growth factors.
- Gene off till complex binded.
- Transcription prevented by protein repressor
molecules.
Hormones to enhance performance
Erythropoietin EPO
* Peptide hormone produced by kidneys.
* Stims formation of red blood cells in bonemarrow.
* Can be made with tech. to treat anaemia.
EPO too high = too much blood = risk of
Testosterone
- Steroid hormone (made from chol) produced in
testes adrenal glands. An androgen.
- Binds to androgen receptors. Modify gene
expression.
- eg. Increase anabolic reactions in muscle cells.
- Injections ineffective as broken down quickly.
So synthetic anabolic steroids manufactured.
- ^ BP, liver damage, v sperm production, kidney
failure,
heart disease.
Unbanned Substances
Creatine. Nutritional supplement. ^ CP in
muscles.
Combined with weight training,
^ muscle mass, v recovery time.
Bad effects. ^ BP, kidney damage, vomiting,
cramps.
Should they be banned? p193
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8.1 Nervous System + Impulses
What Are Nerve Cells Like?
Complex structure containing bundle of axons of
many neurones, with protective coating.
Cell body contains nucleus + cell organelles in
cytoplasm.
Two thin extensions: Dendrites- toward cell
Axon- away from cell
Motor Neurone Cell body in CNS. AKA effector
neurone
Sensory Neurone- Impulses from sensory cells to
CNS.
Same but just dendrites on left, and
Relay Neurone- Mostly in CNS. AKA connector
neurones.
Same as sensory but..
NS
CNS Peripheral NS
Brain + spinal cord Sensory nerves,
Motor nerves
(toeffectors)
ANS
Somatic NS
Involuntary Voluntary
Stim muscle + glands Stim
skeletal muscles
Sympathetic NS Parasympathetic
-Usually fatty, insulating myelin sheath around
axon.
-Made up of Schwann cells wrapped around
axon.
-Not all animals have myelinated axons.
Reflex Arcs
- Nerve impulses follow pathway. Simple ones
are reflex arcs
that produce reflex rapid, involuntary response
to stimuli.
- Most more complex. Sensory > neurones in
CNS > brain.
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Pupil Reflex
Iris controls size. Pair of antagonistic muscles:
Radial- Sympathetic reflex, Circular-
Parasympathetic reflex.
Controlled by ANS.
* Radial relax, circular contract = Constricted
pupil.
* Radial contract, circular relax = Dilated pupil.
Controlling Pupil Size-Light strikes photoreceptors of retina.
- Nerve impulses > optic nerve > CNS.
- Along parasympathetic motor neurones to
circular muscles. Contract + radial relax.
How Nerve Cells Transmit Impulses
Inside a Resting Axon
Pot diff across axon membrane.
Inside axon, -70mV. So inside more neg, so
polarised.
= resting pot
Why is there a pot. diff?
-Diff conc of ions outside + inside, due to Na-K
pumps inmembrane. Go against conc grad using ATP.
- Organic anions (neg charged aminos) stay
inside cell, so
chloride ions move out to balance charge.
Resting Potential
When no diff between inside + outside charge, K
diffuses out down conc grad.
So outside more pos, inside more neg.
Membrane impermeable to most Na+. So,
resting pot.
Why -70mV?
* Conc grad by Na+/K+ pump.
* Electrical grad due to diff in charge.
At -70mV, the electrical grad balances the chem.
one, so no more movement of K+.
Diagram p203
What Happens when a Nerve is Stimulated?
- Pot diff across cell membrane changes when
impulse conducted.
- If electrical current applied, the pot diff across
membrane is reversed: Inside pos, outside neg.= Depolarisation
- Diff becomes +40mV, then returns to resting
=repolarisation
Change in voltage is an action potential.
What causes an action potential?
Caused by changes in permeability of membrane
to Na + K,
due to o en/close of volta e de endent Na + K
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1) Depolarisation 2) Repolarisation
Na+ gate changes shape Na+ channels
close, K+ open
opening channels. due to dep. So K move
out
Na+ flow in, ^dep, down
electrochem grad.
triggers more gates to Inside more
neg.
open, ^dep = pos feedbackAll-or-nothing. 3) Restoring
Resting Pot
^conc of Na outside Membrane ^
permeable
How is the impulse passed along an axon?
Neurone stim, action pot doesnt travel along
but triggers sequence of action pots along axon.
As part of membrane dep, electrical currentcreated as charged Na flow between dep region
and adj. resting region, spreading dep to that
region, triggering another action pot..
Refractory period = Delay where another action
pot. cant be
generated again in same place,
until all voltage dep Na + K close
again +
resting restored.
Ensures impulse only travels in one direction.
Are Impulses Different Sizes?
Same size of action pot. All-or-nothing.
These mechs depend on intensity of stim:
- Freq of impulses
- No. neurones conducting impulses.
Speed of Conduction
Wider axon = faster. Myelin sheath insulates =
faster.
Nodes of ranvier gaps are only place dep can
occur.So impulse jumps from one node to next
= saltatory conduction
How does a Nerve Impulse Pass Between Cells?
- Two neurones meet at synapse. Gap is synaptic
cleft.
Synapse Structure
Presynaptic membrane, cleft, postsynaptic
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How does the synapse transmit an impulse?
Action pot at presynaptic membrane causes Ca+
ions to open. Diffuses into cell.
Causes vesicles to fuse with membrane,
releasing neurotransmitter into cleft by
exocytosis.
Diffuses across gap, causing dep. in post
membrane.
Stim of postsynaptic membrane
- Neurotransmitter binds to receptor molecule,
changing its shape. Opens cation channels so
Na+ flows in, causing dep.
Extent of dep depends on amount of
neurotransmitter + no receptors.
Usually need many impulses for postsynaptic to
be dep.
Inactivation of neurotransmitter
Some taken back up by presynaptic membrane
+ reused.
Others diffuse away.
What is the Role of Synapses in Nerve
Pathways?
Control + Coordination
Synapses... control nerve pathways.
Integrate info from diff neurones.Post. cell receive input from many synapses at
the same time.
Likelihood of dep... Type of synapse, no.
impulses received.
Types of Synapse
Excitatory- Make post. membrane ^ permeable
to Na+
Need many for action pot
(summation)*Spatial summation Impulses from diff
synapses.
*Temporal summation Many impulses, same
synapse.
Inhibitory- v likely action pot will happen:
Neurotransmitter opens cl- and K+
channels,
Cl- goes in, K+ moves out, so ^ pot diff
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Comparing Nervous + Hormonal Coordination
Many hormones produced steadily over time to
control long-term changes in body, eg. growth +
sex dev. eg. testo.
Adrenaline= ST action. But takes longer than NS
to produce a
response.
Nervous Control Hormonal Control-Electrical
transmission by nerve
impulses + chem.
transmission at
synapses.
-Fast acting, ST
-Chem transmission
through blood.
-Slow acting, LT
changes.
- Blood carries
hormone to all cells,
Coordination in Plants
Plants lack NS.
Plant growth substances. eg. Auxins Phototropism- Bending to
light
Auxin made in tip, passed down to coleoptile.
Auxin moves to shaded side of shoot, ^ cell
elongation which bends it towards light.
New research- Gen. mod plants that produce
fluorescent
protein where auxin is.
Auxin synth in meristems (growing tissue)shoot, tip, leaves, seeds, fruits
-Bind with receptors on plasma membranes
> producing second messenger that changes
gene expression> acidification of cell wall (by stim of H+
pumps)
> Low pH affects enzyme in cell wall causing
bonds between microfibrils to break > Cell wall
expands.
^ pot diff + ^ ion uptake into cell = Water
uptake by osmosis
= Cell elongation.
Auxin experiments:
8.2 Reception of Stimuli
How does light trigger nerve impulses?
Receptors
Detect stimuli. Send impulses to CNS.
Some types of receptor cells grouped together in
sense organs eg. eyes.
Helps to protect them + improve efficiency.
S i hi Ph
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Structures within sense organ ensure receptor
cells receive approp stim.
- Light receptors are in eye.
Lens + cornea refract light, focusing it on
retina.
Photoreceptors
Rods - B+W vision in dim + bright light
& cones -Colour vision in bright light
-Centre of retina= Only cones. for detail.
- Elsewhere, rods 20: 1 cones
How does light stim photoreceptor cells?
In rods + codes, photochem pigment absorbs
light.
In rods = Rhodopsin
In the membranes of the vesicles.
In dark: -Na+ diffuses into outer segment
through channels.
-Na+ moves down to inner down conc
grad.
-Na+ actively pumped out.
-Membrane slightly depolarised -40mV
=neurotransmitter released, binding to
bipolar cell,
In light: -Rhodopsin breaks down > Retinal +
Opsin
-Na+ channels closed
-Na+ pumped out
-Membrane hyperpolarised
-No inhib. neurotransmitter released,
so Na+ can enter bipolar cell through
channels
= depolarised = action pot. to optic nerve.
Rhodopsin is reformed.
^ light intensity = more rhodopsin broken down
= longer for it to reform. Reforming = Dark
adapt (?)
Pl l d d Ph h i i i
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Plants can also detect + respond to env cues
- Light is important cue
- Plants detect quantity, direction + wavelength
using photoreceptors.
Eg. Phytochromes absorb red + far red light
Has protein component + non-protein light
absorbing pigment Pr and Pfr
Isomers. Photoreversible.
Plants synth Pr. Absorb red Pfr. Absorb farred Pr.
Pr Pfr happens more in light because there is
more red.
Phytochromes trigger germination
Flash of red light triggers, but if followed by flash
of far-red, inhibs.
Photoperiods, flowering and phytochromes
-Flower at particular time of year
- Photoperiod = relative length of day and night.
Determines flowering.
- Ratio of Pr to Pfr allows it to determine length
of day and
night.
Long day plants- Need less than X amount of
uninterrupted darkness, because need Pfr to
flower.
Short day plants- Need more than 12 hrs
uninterrupted darkness, because need Pr. Need
time to convert Pfr Pr,
as Pfr inhibs.
Needs to be uninterrupted as flash of red in dark negates
effect of dark period
Phytochrome and greening
Greening= When shoot breaks through soil into
sunlight and
plant changes in form and chem.
Inhib elongation of internodes.
How do phytochromes switch process on/off?
- Activated phytochromes interact with other
proteins.
May bind to it or disrupt binding of complex.= Transcription factors / activation of transcrip
factors
Transcription + translation Plants response to
light. eg.
synth enzymes
that control
chlorophyll to green.
Pl t d t t th
H i h t d b hit tt (
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Plants detect other env cues
Gravity- Under soil, light cant stim, so stim for
root + shoot
growth is gravity.
Touch + mech stress- Some plant stems rubbed
grow less.
Some leaves touched
roll in (cells lose
K + water lost by
osmosis = flaccid)8.3 The Brain
Cerebral Hemispheres
Cortex is grey + highly folded. Nerve cells,
Hemispheres connected by white matter (nerve
axons)Corpus
Collosum
Each lobe interprets + manages sensory inputs.
Below corpus collosum..
* Thalamus- Routes incoming sensory info via
white matter.
* Hypothalamus- Thermoreg centre. Core temp,
skin temp.
Sleep, hunger, thirst.
Secretes anti-diuretic
hormone.
* Hippocampus- LTM
Basal ganglia is deep inside hemispheres.
Initiates stored programmes for movements.
Cerebellum + brain stem
Stem extends from midbrain to medulla
Discovering functions of brain regions- p229
Effect of strokes.
Speech problems, reading, writing, lesions in
small area of frontal lobe.
Some recover due to neural plasticity.
Brain Imaging MRI
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Brain Imaging
CT Scans
X rays cant image soft tissue as only absorbed
by denser material, eg. bone.
-Uses narrow beam X rays rotated around the
patient to pass through tissue from diff angles.
- Each beam is attenuated (v strength) according
to tissue density
-X rays detected + used to make image of thin
sline of brain on comp screen.
frozen moment pic. Structure, not function.
Limited resolution.
MRI
Magnetic field + radiowaves detect soft tissue.
- Nuclei of atoms line up with direction of
magnetic field.
- H atoms monitored as ^ water content in
tissues.
- Magnetic field down tube. Another field on this,
from magnetic component of high freq waves.
-Combo causes axis + freq of spin of H nuclei to
change, taking energy from radiowaves.
- When radio off, H nuclei return, releasing
energy.
- Signal to comp Image.
Functional MRI
Human activity, memory, emotion, language.
Used by looking at O uptake of active areas, as
deoxyhaemoglobin absorbs radiowaves. (oxy
doesnt)^ Activity = ^ blood flow as ^ demand for O
Less signal absorbed, higher activity of area.
From Eye to Brain
* Optic nerve extends to brain, inc thalamus.
Impulses then sent to neurones to visual cotex.
* Before thalamus, some neurones of optic nerve
branch to midbrain to motor neurones. Controls
pupil reflex + eye movement.
8.4 Visual Development
Postnanal ^ in brain size caused by elongationof axons, myelination, dev of synapses.
When neurones stop dividing, they move to fixed
positions + wire themselves. Synapse with other
neurones.
Axon Growth
- Axons in retina grow to thalamus, forming
synapse with neurones there.
- Axons from thalamus grow to visual cortex.
Visual cortex made up of columns of cells
So need full range of light stimuli to enter to dev
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-Visual cortex made up of columns of cells.
-Columns next to each other get stim from same
area of retina of left + right eyes.
- Columns formed before birth (found in animals
that received no visual stim)
Critical windows Need specific exp. to dev
properly.
Evidence for crit period in visual dev
Medical Observations-Boy, eyes bandaged 2 wks, Impaired vision.
-Cataracts. Clouded lens. If not removed before
10, permanent impairment.
-
So need full range of light stimuli to enter to dev.
Animal Models
Easy to obtain, breed, short life, small size.
Kittens + monkeys, because similar.
Newborn Animals
Monkeys- Dark, or light but no pattern
Impaired vision
So need patterns.
Monocular deprivation = Deprive one eye
What happens during Crit Period?
At birth, overlap between territories of diff
axons.
Adults, less overlap.- Monocular deprivation, columns for that eye
are narrower as dendrites/synapses from stim
eye take up more territory.
Axons compete for target cells in visual cortex,
as whenever a neurone fires onto target cell,
synapses of another neurone sharing the cell
are weakened and release less neurotransmitter.
8.5 Making sense of what we see
- Some neurones respond to bars of light
simple cells.
- Others respond to edges, slits or bars that
move
Complex cells.- Others respond to angles of edge, contours,
movement, orientation.
-Perception involves memory and exp.
Depth Perception
Close objects
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Distant Objects
>30m. Visual cues + past exps.
+ overlaps of objects, change in colour.
Is Depth Perception Innate?
Cross-Cultural Studies
- Carpeted world hypothesis. Straight lines +
right angles.
Interpret angles.
- Some believe due to genetics. Diffs inpigmentation.
ie. poor contour detection= ^ retinal
pigmentation.
Studies with Newborn Babies
- Inborn capabilities. Eg. Distinguish human
faces
(ev of hardwiring of brain before birth)
- Born short-sighted but prefer patterns, tell diff
between happy + sad face, imitate expressions.
Visual Cliff
Crawl across glass table. The baby stops, so
suggests innate depth perception.8.6 Learning And Memory
Where Memories are Stored
Throughout cortex. Diff sites for ST + LT.
Diff t es of memor controlled diff arts.
HM- Removed part + couldnt form new LT
memories
+ poor ST.
How Memories are Stored
By altering: - pattern of connections- strength of synapses
Sea Slugs + Habituation = Changing synapse
strength
-Giant sea slug breathes through gill. Water
expelled through siphon tube at cavity. If siphon
touched, gill drawn into cavity (Reflex)
- Freq hit by waves + learn not to withdraw gill =
How habituation is achieved:
-Repeated stim of neurone = Ca2+ channels v
responsive.
- So less Ca2+ crosses membrane, so less
neurotransmitter
released.-So less depolarisation, so no action pot. in
motor neurone
for gill.
More connections = Longer memory
-LT memory storage involves ^ no. synaptic
connections.
-Rep use of a synapse creation of additional
8 7 Problems with Synapses Treatment
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8.7 Problems with Synapses
- Imbalances in brain chems cause problems.
- Drugs crossing blood-brain barrier cause
problems.
- Endothelial cells of capillaries are more tightly
joined in brain, forming barrier to control
movement of substances.
Parkinsons Disease
Dopamine + Parkinsons
v secretion of DA. Motor cortex doesnt receiveit, so..
* Stiff muscles
*Muscle tremors
Treatment
-Drugs to slow loss of DA by inhib breakdown.
- Drugs to treat symptoms eg. L-Dopa to ^ DA.
- DA agonists to activate DA receptors triggering
action pot.
- Gene therapy to ^ DA.
Depression
Serotonin + Depression
Neurones secrete it in the brain stem.Axons extend into the cortex, cerebellum, spine.
v serotonin = dep. Sad, anxious, hopeless, v interest, venergy, insomnia,
restless death thou hts.
*5-HTT gene- codes for transporter protein that
controls reuptake of neurotrans into presynaptic
neurones.
*Short version of 5-HTT = more likely to dev
after stressful life event.
*Neurotrans: DA, noradrenaline. Is serotonincause or effect?
*When dep, v nerve impulses transmitted. Low
conc of molecules needed to synth, but ^
serotonin-binding sites (?)
*Twin studies
Drugs for dep:
Inhib reuptake of serotonin from synaptic cleft.
Prozac. Mintains ^ level + ^ rate of impulses in
serotonin pathways
How Drugs Affect Synaptic Transmission
- Some may bind to same receptors.
- Some prevent release.
- Some block/open ion channels.
- Some inhib a breakdown enzyme.p254
diagram
The Effect of Ecstasy
Effects of using Ecstasy
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The Effect of Ecstasy
Derivative of amphetamine.
Affects thinking, mood, memory.
Can cause anxiety + altered perceptions.
ST effects- changes in beh + brain chem
LT effects- changes in beh + brain structure
How Ecstasy affects synapses
^conc serotonin in cleft by binding to molecules
that reuptake.
May cause them to work in reverse (so put more
there)
Effects of using Ecstasy
Stim so much serotonin release that cells cant
synth enough when drug is withdrawn.
Better Treatments
Deciphering base sequences in human genome
as part of Human Genome Project.
How outcomes help:
Finding the sequences
*DNA frags replicated, separated. Base at each
end ID.
* Using sequence ID new genes, how controlled
+ what they code for.
ID of new drug targets
* Drug target = Specific molecule that drug
interacts with.
* Diff side effects exp by ppts diff genes,
depending on which single nucleotide
polymorphisms they have.
*Ethics: Testing for genetic predisp- insurance
companies.
Who should decide use and who to use on?
Making + keeping records- confidentiality.
Using Gen Mod Organisms for Drugs
- Mod orgs to produce human proteins. eg.
Mod microorganism
-Bacteria contain plasmids. Can be transferred
from one cell to another.
-Restriction enzymes cut the plasmid. Enzymes
can insert DNA from another species.
-Plasmid put back into bacteria. Multiply infermenter.
- Protein produced extracted from culture.
Gen Modified Plants Not always successful, so incorp a marker gene
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Gen Modified Plants
Artificial selection= Choosing particular plants to
save seeds
+ sow next year, so they
improve.
Selects alleles for good chars.
Gen mod crops can mass produce meds +
chems. Eg proteins to heal wounds or conds.
-Foreign gene inserted by.. Bacterium that
infects plant(plasmids)
- Small pellets
Not always successful, so incorp a marker gene
to see if the gene is actually present afterwards.
(Gene for antibiotic resistance youre modding
for)
*Plant then incubated with antibiotic, killingcells
that dont contain the marker.
Surviving cells have the new gene
*Gen mod plant cultured in agar to make new
plants= MIcropropagation
Gen mod animals
Inject DNA into nucleus of fertilised egg. or use
retrovirus
Implant into surrogate.
-AAT made by liver. Inhib enzyme elastase, a
protease that digests ageing lung cells. Released
from neutrophils.
AAT stops it attacking normal tissue.
-Can produce proteins in milk of gen mod
mammals.
Concerns About Gen Mod
Health Concerns:
-
-The GM crops contain the antibiotic resistant
gene as a marker gene. Could be transferred to
microbes in the gut. So need to be removed.
- Concerns that viruses that infect animals could
be transferred to humans in products from genmod animals.
Env issues:
- Transfer of genes to non-GM plants
- ^ chems used in crops.
*Cross pollintation from plants. Could end up
with superweeds
* ..Could make pollen not contain the mod gene,
or make mod cro s infertile