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 units

Light band= Actin. Dark band= Myosin+Actin . Medium= Myosin.

How Sarcomere shortens - Sliding Filament Theory- Nerve impulse arrives at neuromuscular junction. - Ca ions released from sarcoplasmic reticulum.
Diffuse through sarcoplasm

- So head returns to upright position. Many myosin heads nodding = many movements of actin, causing muscle contraction.

- 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 actin moves over myosin. 7.2 Energy for Action BMR = min energy requirement at rest to fuel basic metabolic processes. Prop. to body SA. Releasing Energy Carbs + 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. - so ATP in water stores chem. pot. energy.

When muscle relaxes, not stim by nerve impulses, and Ca pumped out of sarcoplasm using ATP. Troponin and myosin move back.
In rigor mortis, no ATP so cross bridges still attached

ATP in water ADP + hydrated Pi + energy Carb Oxidation C6H12O6 + 6O2 6CO2 + 6H2O + energy - In aerobic resp, H in glucose bonds with O to form water again. Energy release , to generate ATP. - Glucose + oxygen not brought together directly as too much energy too quickly. So, glycolysis.

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 energy
for 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)

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. *H+ diffusion down stalked ATP particle allows 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 grad used 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 in manometer moves up.

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 protein channels. * ATP synthesis catalysed. * H cause conformational change in the ATPase active site, - 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. = point inhib. End product inhibs earlier

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. 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. -Later, creatine phosphate regenerated from ATP

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.

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 consumption and theoretical had 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 completely, but in exercise more residual blood

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 output, ^ breathing rate, deeper 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.

SAN (sinoatrial node) in right atrium (pacemaker) Across Atria (atrioventricular node) Contract (systole) finished ventricles have filled Purkyne fibres Large muscle fibres that conduct impulses to tip * 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. AVN Delay so atria contracting and

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)

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.

- 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 peristalsis.

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) Breathing Tidal Volume = Vol air breathe in and out in one breathe. Vital capacity = Max tidal volume. Measured with spirometer. 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.

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

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 All muscle fibres are not the same Slow Twitch- Dark as a lot of myoglobin. ^ mitochondria, ^ respiratory enzymes For slower, sustained contraction. 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,

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.

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 aerobic.

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. Heat Loss Centre Heat Gain Centre

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 to hypothalamus.

Stim- Sweat glands Stim- Arterioles constrict Inhib-Hair erector -Contraction of arterioles -Liver ^ metabolic rate (dilate capillaries) -Skeletal muscles contract -Hair erector muscles (shiver) (hairs lie flat) Inhib- Sweat glands -Liver (v metabolic rate) -Skeletal muscles (no shivering) -Shivering = uncontrolled contraction of usually

* 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

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, then replaced by colder air, warmed.. (layer of still air
reduces it)

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

Evaporation- Convert water to vapour. Sweating. 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) VigorousDuring recovery these fall: Nat killers, phagocytes, B cells, T helpers. 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, anti-inflamm

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. 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. Type 2 diabetes as sugary food

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.

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 artificially enhancing 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.

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. * 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. - So, receptor, then activates molecule in

Gland Pituitary

Function Stim growth Controls testes + Ovaries. Reabsorption of water in kidneys. Thyroid Thyroxine ^BMR Ovary Oestrogen Promote dev of Ovaries + 2ndry Fem. chars. Testis Testosterone Dev of 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.

Hormone Growth Follicle stim Antidiuretic

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. Attach to promoter region or transcription 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.

Hormones to enhance performance Erythropoietin EPO * Peptide hormone produced by kidneys. * Stims formation of red blood cells in bone marrow. * Can be made with tech. to treat anaemia. EPO too high = too much blood = risk of thrombosis. 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

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 Brain + spinal cord Motor nerves
effectors)

Peripheral NS Sensory nerves,

(to

-Usually fatty, insulating myelin sheath around axon. -Made up of Schwann cells wrapped around axon. -Not all animals have myelinated axons. Reflex Arcs

ANS Somatic NS Involuntary Stim muscle + glands skeletal muscles Sympathetic NS Voluntary Stim

- 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.

Parasympathetic

Pupil Reflex Iris controls size. Pair of antagonistic muscles: Radial- Sympathetic reflex, CircularParasympathetic 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. Constricts pupil, v light entry. 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

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 in membrane. Go against conc grad using ATP. - Organic anions (neg charged aminos) stay inside cell, so chloride ions move out to balance charge. 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 open/close of voltage dependent Na + K

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 feedback All-or-nothing. 3) Restoring Resting Pot ^conc of Na outside Membrane ^ permeable 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.

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 current created as charged Na flow between dep region and adj. resting region, spreading dep to that region, triggering another action pot.. This wave is the nerve impulse. 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 membrane

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

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 -Chem transmission transmission by nerve through blood. impulses + chem. -Slow acting, LT transmission at changes. synapses. - Blood carries -Fast acting, ST hormone to all cells, Auxin synth in meristems (growing tissue)
shoot, tip, leaves, seeds, fruits

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 experiments:

-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.

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.

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, preventing depolarising. Inhib- Glutamate

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 (?)

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. red Pr. Absorb red Pfr. Absorb far

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.

Pr Pfr happens more in light because there is more red. So in light there is more Pfr. 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

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.

Phytochrome and greening Greening= When shoot breaks through soil into sunlight and plant changes in form and chem.

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, synapses, dendrites. (grey matter) 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

Hemispheres connected by white matter (nerve axons)

Corpus Collosum

Each lobe interprets + manages sensory inputs.

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 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. 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.

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. * 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 elongation of 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. -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. - In older ppl, vision normal if removed. What happens during Crit Period? At birth, overlap between territories of diff axons.

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

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 <30m. Stereoscopic vision. Both eyes. 2 angles.

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 in pigmentation. ie. poor contour detection= ^ retinal pigmentation. Depth cues not innate. Learned. 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 = habituated

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 types of memory controlled diff parts. 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 synapses.

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 receive it, so.. * Stiff muscles *Muscle tremors *Slow movement *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 serotonin cause or effect? *When dep, v nerve impulses transmitted. Low conc of molecules needed to synth, but ^ serotonin-binding sites (?) *Twin studies

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.
energy, insomnia, restless, death thoughts. Sad, anxious, hopeless, v interest, v

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

Disrupts synapse.

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. 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 in fermenter. - Protein produced extracted from culture.

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. Growth hormone, insulin, collagen.

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)

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

- Small pellets covered with DNA 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: - Transfer of antibiotic resistance genes to

-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 gen mod 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 crops infertile