bio notes 2

8/6/2019 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,


12/28

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.


13/28

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.


14/28

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


15/28

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.


16/28

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


17/28

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


18/28

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


19/28

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


20/28

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


21/28

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 (


22/28

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

bio notes 2

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