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ahhhhhh 2 Flashcards

1
Q

regulating mucus water content: excess water (5 steps)

A
  1. Na+ actively pumped across the basal membrane out of the cell into tissue fluid making a concentration difference between mucus and cell.
  2. Na+ diffuses through sodium channel (ENaC) in apical membrane into cell down concentration gradient.
  3. electrical gradient between tissue fluid and mucus. Cl- diffuses down electrical gradient from mucus between cells to tissue fluid
  4. water is drawn out of cell in tissue fluid by osmosis due to high salt conc. in tissue fluid
  5. water is drawn out of mucus by osmosis into cell down concentration gradient.
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2
Q

regulating mucus water content: too little water (5 steps)

A
  1. Cl- from tissue fluid is pumped into cell across basal membrane
  2. Cl- diffuses through the open CFTR channel into mucus down concentration gradient.
  3. Na+ diffuses down electrical gradient from tissue fluid into mucus via gap between cells
  4. elevated salt concentration in mucus draws water out of the cell by osmosis
  5. water is drawn into cell by osmosis
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3
Q

regulating mucus water content: CF lungs

A
  1. CFTR channel is absent or not functioning
  2. Na+ channel is permanently open allowing Na+ to diffuse into cell
  3. Na+ is pumped out of the cell into tissue fluid
  4. Cl- down electrical gradient into tissue fluid
  5. water is continually removed from mucus by osmosis
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4
Q

what is the result of water being continually removed from the mucus in CF lungs

A

mucus is too sticky and cant be moved by cilia

  1. mucus to build up effecting ventilation of aveoli
  2. mucus becomes infected with bacteria
  3. phagocytic cells that kill pathogens are produced
  4. phagocytes break down releasing DNA which makes the mucus even more sticky
  5. causing airway inflammation and lung damage
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5
Q

what is the evidence for the fluid mosaic model

A
  • experiments showed types of proteins could dissociated from the membrane and others that could not. this supports fluidity and the fact there are some peripheral proteins and some integrated proteins
  • freeze-fracture electron microscopy fractured between the lipid layer to show that the inner surface was a smooth mosaic interspersed with large proteins.
  • plant proteins lectins bind to polysaccharides labled and when mixed with membrane lectins only bond to the outer surface membrane showing polysacharides where on outside.
  • fusing mouse and human cells after 40 mins protein completely intermixed showing components are fluid
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6
Q

the experiment to prove DNA replication is semi conservative

A
  • DNA either replicates fragmentary, semi conservatively or conservatively.
  • melso and stah grow escherichia coli DNA bacterium in medium contain heavy isotope N15 alll nucleotides contain heavy nitrogen making DNA more dense.
    bacteria then moved to medium containing normal N14 all new nucleotides light.
    bacteria allowed to divide once. DNA then extracted and centrifuged producing a bond of medium density DNA so DNA did not replicate conservatively
    if allowed to undergo a second division producing a strand of medium DNA and one light band of DNA proving DNA did not replicate fragmentary
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7
Q

stages in atherosclerosis

A
  1. endothelium becomes damaged and dysfunctional
    edothelium becomes damaged and dysfunctional. resulting in high blood pressure. putting extra strain on cells.
  2. inflamatory response
    white blood cells move into artery wall. they accumalate chemicals such as cholesterol. a fatty deposit builds up called an atheroma
  3. plaque is formed
    calcium salts and fibrous tissue build up at the site resulting in hard swelling called plaque. artery wall loses elasticity and hardens.
  4. lumen becomes narrower
    making it more difficult to pump blood
    and leads to a rise in blood pressure
  5. feedback
    plaque –> rise in blood pressure —> damage to edothelium —> plaque
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8
Q

what are the stages in the blood clotting cascade

A
  1. plaque reptures exposing collagen to the blood
  2. platelets and damage tissue release a protein called thromboplastin
  3. thromboplastin activates enzyme that catalyses convertion of protein prothrombin into enzyme called thrombin. protein, vitamin k and calcium must be present
  4. thrombin then catalyses conversion of soluble plasma protein, fibrinogen insoluble fibrin.
  5. a mesh of fibrin forms that traps more platelets and red blood cells to form a clot.
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9
Q

name the steps in fertilisation

A

1.the acrosome reaction
when the front of the sperm touches the zona pellucida of the egg the acrosome bursts and releases enzymes which digest a channel in the zona pellucida
2. membrane fusion
the surface membranes of the sperm and egg fuse together allowing the haploid nucleus from the sperm to enter the cytoplasm of the egg
3. cortical reaction
vesicles inside the egg called cortical granules fuse with the cell membrane and release their contents. these cause changes in the surface layer of the egg preventing other sperm from entering
4. meiosis is restarted
the egg is really a secondary ocyte and the presence of the sperm cell causes the 2nd division and meiosis to now occur
5. fertilisation
the chromosomes from the haploid egg and sperm combine to restore the diploid number

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10
Q

what is the lac operon model

A

prokaryote escherichia coli.
only produce the enzyme beta- galactosidase to break down carbohydrate lactose when present in surroundings converts disaccharide lactose to monosaccharides glucose and galactose

when lactose is not present a lactose repressor molecule bonds to the DNA to prevent transcription of beta-glaactosidase gene.
RNA polymerase cannot bind to the DNA promoter region.
when lactose is present it binds to the repressor preventing it from binding to the DNA and the gene is transcribed

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11
Q

evolution by natural selection

A
  1. introduction of selection pressure caused by change in environment, competition or predators.
  2. random mutations produce new alleles which is advantageous. this is caused by natural genetic variation
  3. individuals with the advantageous allele survive and reproduce.
  4. advantageous allele is passed on.
  5. there is a increased frequency of the advantageous allele in the population / gene pool.
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12
Q

taxonomic hierarchy

A

series of taxa which members all share one or more common feature

  1. kingdom
  2. phylum
  3. class
  4. order
  5. family
  6. genus
  7. species
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13
Q

types of kingdoms

A
  1. animali
    muticellular eukoryates that are heterotrophs
  2. plantae
    muticellular eukoryates that are autotrophs
  3. fungi
    muticellular eukoryates that are heterotrophs or absorb nutrients from decaying matter
  4. protoctista
    eukaryotes that photosynthesis or feed on organic matter
    but not included in other kingdoms
  5. prokyaryotae
    prokaryotic organisms
  6. chromista
    includes some groups of fungi plantae and protoctista. which all have tinsel like flagella. the shared features between them make them more closely related to each other than any other kingdom
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14
Q

what are plant cell walls made of

A

cellulose. which is a polymer of alpha and beta glucose.
each chain contains 1000 - 10000 units. straight chain. H bonds form between OH groups of neighbouring chains forming bundles called microfibrils which are about 60 -70 cellulose molecules wound in helical arrangement stuck together with polysacharide glue
hemicellulose and pectins

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15
Q

what are the steps in mass transport

A
  1. photosynthetic products are actively loaded into phloem increasing solute concentration. which draws water into sieve tubes by osmosis from adjacent xylem vessels
  2. this increases hydrostatic pressure at loading end
  3. at sink, solutes are unloaded lowering hydrostatic pressure. the difference in pressure between loading and unloading site causes mass flow along the sieve tube from high to low pressure
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16
Q

medications for treating CHD (5)

A
  • ACE inhibitors
    reduce synthesis of angiotensin II which is a hormone that causes vasoconstriction so lowers blood pressure.
  • calcium channel blockers
    block calcium channels in muscles lining arteries. stopping them from contracting. lowering blood pressure. fatal with someone with heart failure
    -diuretics
    increase volume of urine riding the body of excess fluids and salts decreasing blood plasma volume lowering blood pressure
  • antihypersentive beta blockers
    prevents stimulation of adrenergic receptors responsible for increase cardiac action. control hear rhythm and treat angina as well as reducing high blood pressure.
  • amticoagulant and platelet inhibiting drugs
    asprin and clopidogrel reduces stickness of platlets.
    walfrin interfers with vitamin K affects synthesis of clotting factors.
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17
Q

carbohydrates

A

monomers
-glucose, galactose, fructose
disaccharides
- sucrose: glucose + fructose
- maltose: glucose + glucose
- lactose: glucose + galactose
polysaccharides
- starch: amylose (straight) and amylopectin (branched)
- glycogen: animals. numerous side branches
- cellulose. alpha and beta glucose. microfilis is bundles of cellulose joined by H bonds and microfibrils are held together by hemicellulose and pectin

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18
Q

properties of water

A

solvent:
dissolve other polar and ions
allowing biochemicals reactions to occur in cytoplasm. dissolve substances transported in blood/lymph or xylem/phloem. to enable transport lipids must combine with proteins forming lipoproteins
thermal properties
- high specific heat capacity
strong H bonds. water warms and cools slowly. useful for organisms avoid rapid changes in internal temperature. aquatic life
cohesion: hydrogen bonds between water molecules.
adhesion: Hydrogen bonds between water and cell wall
capillary action
density and freezing points
water expands when frozen as when molecules slow down the max number of hydrogen bonds can form holding them further apart. ice less dense than water.

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19
Q

stages in the sliding filament theory (7)

A
  1. Ca2+ attaches to the troponin molecules causing them to move
  2. as a result tropomyosin shifts exposing myosin binding sites
  3. myosin heads bind with these sites forming cross bridges
  4. when myosin head binds to actin. ADP and Pi on head are released
  5. myosin changes shape, causing myosin head to nod forward. resulting in relative movement of filament attached actin moves over the myosin
    ATP binds to myosin head causing it to detach from the actin
  6. ATPase on myosin head hydrolyses ATP forming ADP + Pi.
  7. this hydrolysis changes shape of myosin head returns to upright position.
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20
Q

how does the nerve impulse trigger the contraction of muscle

A

when a nerve impulse arrives at a neuromuscular junction calcium ions Ca2+ are released from the sarcoplasmic recticulum.
the Ca2+ diffuses through the sarcoplasm
this initiates the movement to the protein filament leading to muscle contraction
when there is no more nerve impulse the muscles relaxes
Ca2+ are actively pumped out of the muscle sarcoplasm, using ATP.
troponin and tropomyosin move back blocking the myosin binding site on the actin.

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21
Q

how does ATP release energy

A

ATP(aq) —-> ADP(aq) + hydrated Pi + energy
ATP in water is at a higher energy level than ADP and PI
ATP in water has chemical potential energy
a small amount of energy is required to break the bond holding phosphate to ATP. once removed Pi becomes hydrated.
a lot of energy is released as bond form between water and phosphate
it requires energy to separate Pi from water to make ATP

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22
Q

glycolysis (4 steps)

A

first step in respiration
1. 2 Pi are added to the glucose from 2ATP molecules increasing glucose reactivity
2. glucose splits into 2 phosphorylated 3 carbon compounds
3. each intermediate is oxidised producing 3 carbon pyruvate. 2 H are removed and are taken up by co enzyme NAD producing reduced coenzyme NADH
4. Pi from intermediate compound transfers to ADP creating ATP along with the energy produced when glucose goes to pyruvate as it is at a higher energy level.
overall reactions :
glucose ———–> 2 intermediate phosphorlated 3 carbons
2 ATP ———–> 2 ADP

2 intermediate ————-> 2 pyruvate + 4 Hydrogens
4ADP + 2 Pi (from pyruvate) —–> 4ATP
4H + 2NAD —–> 2 NADH
net yield:
- 2 ATPs
- 2 pairs of H = 4 Hydrogens
- 2 3 carbon pyruvate
2H + coenzyme NAD —> reduced coenzyme NAD
- 2 NADH / reduced coeNAD

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23
Q

what happens to pyruvate in the link reaction

A

pyruvate is
- de carbozylated (Co2 released as a waste product)
- de hydrogenated (2 Hydrogens are removed and taken up by coenzyme NAD
resulting in 2 carbon molecule which combines with coenzyme A to form acetyl co enzyme A (acetyl CoA)
pyruvate + NAD + CoA –> Acetyl CoA + reduced NADH + CO2

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24
Q

what are the 4 important types of reaction that occurs in the krebs cycle

A
  • phosphorylation reactions. which add a phosphate e.g ADP + pi —> ATP
  • decarboxylation reactions, which break off CO2
  • dehydrogenation. (redox reaction) molecule which gains H is reduced
    molecule that loses H is oxidised
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25
Q

what happens in the Krebs cycle

A
  • each 2c acetyl CoA combine with 4 carbon compound creating 6 carbon compound
  • in a circular pathway the original 4 carbon compound are recreated
  • 2 steps involve decarboxylation
  • 4 steps involve dehydrogenation
  • 1 step involves substrate level phosphorylation with direct synthesis of ATP
    hydrogen produce turn FAD / NAD into reduced NAD / FAD
    net yield:
    2 acetyl CoA go in
    produces
  • 2 ATP
  • 6 reduced NAD / NADH
  • 2 reduced FAD
  • 2 CO2
  • reformation of the 4 carbon intermediate
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26
Q

stages in the electron transport chain (6)

A
  1. reduced Co enzyme carries 2H+ and 2e- to electron transport chain on inner mitochondrial membrane
  2. e- pass from 1 electron carrier to the next in a series of redox reactions
  3. H+ move inter membrane space creating high H+ conc.
  4. H+ diffuses back into mitochondrial matrix down electron chemical gradient
  5. H+ diffusion allows ATP synthases to catalyse ATP synthesis.
  6. e- and H+ recombine to form H which combines with O2 to create water.
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27
Q

chemiosmotic theory (4) ATP production from electron transport chain

A
  1. energy is released as electron pass down electron transport chain
  2. this energy is used to move H+ from matrix into intermembrane space creating an electrochemical gradient making intermembrane space more positive than matrix
  3. H+ diffuses down electrochemical gradient through protein channels with ATP synthase causing a conformational change enabling the ADP and Pi to bind with active site
  4. within matrix H+ and e- recombine and combine with oxygen to form water. oxygen acting as the final carrier of the electron transport chain
28
Q
  1. number of ATP molecules made per glucose molecule

2. how many ATP can be made from reduced NAD / reduced FAD

A
  1. 1 glucose molecule produces a net yield of 38 ATP
  2. each reduced NAD results in 3 ATP
    each reduced FAD results in 2 ATP
29
Q

how is respiration controlled by ATP

A

ATP inhibits enzymes involved in glycolysis
- the phosphorylation of glucose
- the enzyme responsible can exist in 2 different forms
- in the presence of ATP enzyme has a shape that makes it inactive
- as ATP is broken down, the enzyme is converted back to the active form and catalysis phosphorylation of glucose
end point inhibition
then end products inhibits early step in the metabolic pathway controlling processes.

30
Q

anaerobic respiration
how is lactate removed
oxygen debt

A

it is possible to oxidise the reduced NAD created during glycolysis in absence of oxygen
- pyruvate produced at the end of glycolysis is reduced to lactate and oxisides form of NAD is regerated
continue to break down glycose to make a small amount of ATP
net yield: 2 ATP per glucose 2% efficiency

lactate is converted back to pyruvate
it is oxidised directly to CO2 and H2O via Krebs cycle releasing energy to synthesis ATP
as a result O2 uptake is greater than normal in recovery period
excess oxygen requirement which is needed to fuel oxidation of lactate

31
Q

ATP / Pc system. supplying instant energy

A

creatine phosphate —> creatine + Pi
ADP + Pi —> ATP
creatine phosphate (Pc) is hydrolysed to release energy
energy used to regenerate ATP from ADP and Pi provided by Pc
Pc is broken down as soon as exercise begins triggered by formation of ADP
does not require oxygen and provides 6 - 10 seconds of intense exercise. later Pc is regenerated from ATP

32
Q

steps in hear muscle contraction (3)

A
  1. SAN generates electrical impulse which spreads across the atria causing them to contract
  2. impulse travels to AVN. slight delay through non conducting cells ensuring atrias finish contacting
  3. signal reaches the purkyne fibres conduct impulse to the ventricular muscle depolarising at the apex ventricular cells and going upwards causing contraction moving up ventricles pushing the blood into the aorta and pulmonary artery
33
Q

what are the 2 nerves going from the cardiovascular control centre to the heart

A
  • a sympathetic nerve (accelerator)
    this raises the heart rate. increases venous return, which leads to a rise in stroke volume, resulting in higher cardiac output, thus transporting oxygen and fuel more quickly
  • vagus nerve, parasympathetic. (decelerator)
    does the opposite
    the cardiovascular control centre located in the medulla oblongata, controls the heart rate via nervous system can detect:
  • the accumulation of CO2 and lactate in the blood, increased oxygen and increased temperature
  • sent impulses from sensory receptors in muscles detecting mechanical activity in muscles.
34
Q

adrenaline

A

adrenaline is a hormone produced by the adrenal glands located above the kidneys
direct affect on SAN increasing heart rate to prepare the body for fight / flight.
causes dilation of the arteries supply skeletal muscles
constricts arteries going to the digestive and other non essential organs, this maximises blood flow to the active muscles
increases heart rate.

35
Q
  1. what happens during inhalation

2. what happens during exhalation

A
  1. ventilation centre sends nerve impulses every 2-3 seconds to external intercostal and diaphragm muscles which contract causing inhalation
    during deep inhalation, not only are the external intercostal and diaphragm muscles stimulated but upper chest and neck muscles are also stimulated
  2. stretch receptors in bronchioles stimulated which send inhibitory impulses to ventilation centre
    impulses to muscles stops and muscles relax
    elastic recoil of the lungs and with the help of gravity lowers the ribs
36
Q

what happens to breathing when CO2 in the blood increases

A
  • CO2 dissolves in blood making carbonic acid H2CO3 which dissociates to H+
    CO2 + H2O –> H2CO3 –> H+ + HCO3-
  • chemoreceptors sensitive to H+ / pH located in ventrilation centre of the medulla oblongata detect H+ concentration increase / pH decrease
  • impulses are sent from the ventilation centre stimulating breathing muscles. increasing rate and depth of breathing
37
Q

differences between slow and fast twitch fibres (6)

A

S- slow F- fast

  • S is red because it has lots of myoglobin F is white because it has few myoglobin
  • S has lots of mitochondria. F has few
  • S little sarcoplasmic recticulum where as F has extensive sarcoplasmic reticulum
  • S has low glycogen content. F has high glycogen content
  • S has numerous cappilaries. F has few capillaries
  • S is fatigue resistant and F fatigues quickly
38
Q

how is testosterone concentration controlled by negative feedback

A

testosterone concentration change detected by hypothalamus
a decrease causes gonadotrophin releasing hormone to be produced by the hypothalamus
this stimulates the pituirity gland to release hormones that stimulate the testes to synthesise testosterone

39
Q

theremoregulation

  1. the heat loss centre in the hypothalamus
  2. heat gain centre
A
  1. control of reducing body temperature to norm
    stimulates: sweat glands to secrete sweat
    inhibits:
    - contraction of arterioles in skin (dilating capillaries in the skin
    - hair erector muscles relax
    - liver (reduces metabolic rate
    - skeletal muscles relax.

2.controls the processes that increases heat gain to normal temperature
stimulates:
- arterioles in the skin to constrict
- hair erector muscles to contract
- liver to raise metabolic rate
- skeletal muscles to contract in shivering
inhibits
- sweat glands

40
Q
  1. vasoconstriction

2. vasodilation

A
  1. in colder conditions the muscles in the arterioles wall contract.
    causing the arterioles to constrict reducing blood supply to the surface capillaries
    blood diverted through shunt vessel which dilates to allow more blood.
    blood flows further from the skin surface so less energy is lost
  2. in warm conditions the shunt vessel constricts and muscles in wall of the arterioles relax
    blood flows through the arterioles making them dilate. more blood flows closer to the surface so more energy is lost
41
Q

arragnement of muscle fibres within muscles

A
  1. tendons at each end connect muscle to bone
  2. muscle is made up of bundles of muscle fibres up to 2cm across. bound together by connective tissue
  3. each muscle fibreis a single muscle cell
  4. each muscle fibrire may be several cm long but less than 0.1 mm in diameter
  5. inside muscle fibre is cytoplasm containing organelles. contain numerous myofibrils each composed of repeated contractile units called sacromere.
42
Q

what are the advantages of physical activity (7)

A
  1. increases atrial vasodilation lowers blood pressure reduces risk of CHD and stroke
  2. increase blood HDLs reduce LDL associated with development of atherosclerosis
  3. helps maintain healthy weight balance energy input = energy output
  4. increases sensitivity of muscle cells to insulin improving blood glucose regulation decreasing type 2 diabetes
  5. increases bone density delaying onset of bone wasting
  6. reduces risks of some cancer
  7. improves mental well being.
43
Q
  1. peptide hormones

2. steroid hormones

A
  1. protein chains not able to pass through cell membrane because of charge
    - instead bind to receptor on the cell membrane which activates another molecule in the cytoplasm,
    - the functional second messenger brings about chemical changes in cell directly or indirectly by affecting gene transcription.
    EPO, human growth hormone and insulin
  2. formed form lipids have complex ring structure
    pass through the cell membrane and bind directly to a receptor molecule in cytoplasm
    hormone receptor complex brings about characteristic response resulting from its effect on transcription . transcription factor.
44
Q

what happens in a reflex arc

A
  1. receptors detect a stimulus and generate a nerve impulse
  2. sensory neurones conduct a nerve impulse to the CNS along a sensory pathway
  3. sensory neurone enters the spinal cord through the dorsal route.
  4. sensory neurone forms a synapse with a relay neurone
  5. relay neurone forms a synapse with a motor neurone that leaves the spinal cord through the ventral route
  6. motor neurone carries impulses to an effector which produces a response.
45
Q

how is pupil size controlled

A
  • high levels of light striking photoreceptors in the retina cause nerve impulses to pass along the optic nerve to a number of different sites within the CNS, including a group of coordinating cells in the midbrain.
  • impulses from these cells are sent along parasympathetic motor neurones to the circular muscles of the iris, causing them to contract. as the radial muscles relax. this constricts the pupil reducing the amount of light entering the eye
46
Q

how is the resting potential maintained

A
  1. Na+ / K+ pump creates concentration gradient across the membrane.
  2. K+ diffuse out of the cell down the K+ concentration gradient, making the outside of the membrane +ve and the inside -ve creating a potential difference
  3. the potential difference will pull K+ back into the cell as it diffuses down the electrical gradient
  4. at 70- mV potential difference, the 2 gradients counteract each other and there is no net movement of K+
47
Q

action potential

summarised

A
  1. depolarisation. all nor nothing. voltage dependent Na+ channels open. Na+ flow into axon depolarising the membrane
  2. repolarisation. voltage dependent Na+ channels close. voltage dependent K+ channels open. K+ leave the axon, repolarising the membrane
  3. restoring resting potential. the membrane is hyperpolarised. voltage dependent K+ channels close. K+ diffuse back into the axon to recreate the resting potential.
48
Q

how is the impulse passed along an axon

A
  1. at resting potential there is +ve charge on outside and -ve on inside of membrane with high Na+ conc on outside and high K+ concentration on inside
  2. when stimulated, voltage dependent Na+ channels open, Na+ flow into the axon depolarising membrane. localised electric currents are generated in the membrane. Na+ move to the adjacent polarised (resting) region causing a change in the electrical charge (potential difference) across this part of the membrane
  3. the change in potential difference in membrane adjacent initiates second action potential. at the site of first action potential the voltage dependent Na+ ions close and voltage dependent K+ channels open K+ ions leave axon polarising membrane becomes hyperpolarised
  4. a 3rd action potential is initiated by the second. in this way local electrical currents cause the nerve impulse to move along the axon. at the site of the first action potential, K+ diffuse back into the axon, restoring the resting potential.
49
Q

refractory period

A

the new action potential cannot be generated in the same selection of membrane for about 5 milliseconds. this is known as the refractory period, which makes sure that the impulses travels in one direction along a nerve fibre.
lasts until all the voltage dependent Na+ and K+ channels have returned to their normal resting state (closed) and the resting potential is restored. the refractory period ensures that impulses only travel in one direction.
a new action potential will only be generated at the leading edge of the previous one; because the membrane behind it will be recovering / incapable of transmitting an impulse; the membrane has to be repolarised and return to resting potential before another action potential can be generated.

50
Q

stages in synaptic transmission

A
  1. an action potential arrives at the presynaptic membrane
  2. the membrane depolarises. calcium (Ca2+) ions channels open. Ca2+ enters the neurone
  3. Ca2+ cause synaptic vesicles containing neurotransmitter to fuse wit the presynaptic membrane.
  4. neurotransmitter is released into the synaptic cleft (exocytosis) it takes 0.5 ms to diffuse across the synaptic cleft and reach the postsynaptic membrane.
  5. neurotransmitter binds with complementary receptors on the postsynaptic membrane. cation channel open. sodium ions Na+ flow through the channels.
  6. the membrane depolarises and initiates an action potential.
    extent of depolarisation depends on amount of neurotransmitter reaching the postsynaptic membrane. depends on frequency of impulses reaching the presynaptic membrane and the number of functioning receptors in the postsynaptic membrane.
  7. when released from the receptor the neurotransmitter will be taken up across the presynaptic membrane (whole or after being broken down) or it can diffuse away and be broken down.
51
Q
  1. excitatory synapses

2. inhibitory synapses

A
  1. make the postsynaptic membrane more permeable to sodium ions.
    as single excitatory synapse typically does not depolarise the membrane enough to produce an action potential, but several impulses arriving within a short time produce sufficient depolarisation via the release of neurotransmitter to produce an action potential in the postsynaptic cell.
  2. make it less likely that an action potential will result in the postsynaptic cell.
    the neurotransmitter from these synapses opens channels for chloride ions and potassium ions in the postsynaptic membrane, and these ions will then move through the channels down their diffusion gradients.
    chloride ions will move into the cell carrying a -ve charge and K+ ions will move out carrying a +ve.
    greater potential difference across the membrane as the insides become more negative than usual (about -90 mV)
    this is called hyperpolarisation.
    this makes subsequent depolarisation less likely. more excitatory synapses will be required to depolarise the membrane.
52
Q

what is the differences between nervous control and hormonal control (5)

A
  1. NS - electrical transmission by nerve impulses and chemical transmission at synapses
  2. HS - chemical transmission through blood
  3. NS- faster acting
  4. HS- slower acting
  5. NS- usually associated with short term changes
  6. HS- can control long term changes
  7. NS- action potential carried by neurones with connections to specific cells
  8. HS- blood caries the hormones to all cells, but only target cells are able to respond.
  9. NS- response is often very local, such as a specific muscle cell or gland
  10. HS- response may be widespread, such as growth and development.
53
Q

how does auxin bring about cell expansion

A

to bring about cell expansion requires a loosening of the cell wall, it is thought that auxin causes the acidification of the cell wall by stimulating the activity of proton pumps that move H+ ions out of the cytoplasm and into the cell wall.
here, the low pH activates proteins called expansions. these expansins disrupt the bonds that hold the cellulose microfibrils and hemicelluloses together.
there is loosening of the cell wall: there is slippage of the polysaccharides relative to each other, bonds reform in new locations, allowing expansion of the cell.
other plant hormones and non enzymatic proteins are also involved in a complex sequence of extracellular and intracellular changes.
the acidification of the cell wall increases the potential differences across the membrane, this enhances the uptake of ions into the cell. in turn, the presence of these ions causes water uptake by osmosis, causing the cell to swell resulting in cell elongation.
plant growth involves cell division and enlargement. in the meristem, cells are actively dividing, most of these cells then enlarge, forming a region of elongation adjacent to the meristem. these cells go on to mature and differentiate.

54
Q
  1. rod cells in the dark

2. rods cells in the light

A
  1. Na+ flow into the outer segment through non specific cation channels. the Na+ move down the concentration gradient into the inner segment where pumps continuously transport them back out of the cell.
    the influx of Na+ produces a slight depolarisation of the cell.
    the potential difference across the membrane is about -40 mV, compared with the -70 mV resting potential.
    this slight depolarisation triggers the release of a neurotransmitter thought to be glutamate, from rods ells.
    in the dark the rod cells release this continuously.
    the neurotransmitter then binds to the bipolar cell, stopping it depolarising.
    • when light falls on the rhodopsin molecule, it breaks down into retinal and opsin, non protein and protein components.
      - the opsin activates a series of membrane bound reactions, ending in hydrolysis of a cyclic nucleotide molecule attached to the cation channel in the outer segment.
      - the breakdown of this molecule results in the closing of the cation channels. the influx of Na+ into the rod decreases, while the inner segment continues to pump Na+ out.
      - this makes the inside of the cell more negative. it becomes hyperpolarised and the release of the glutamate neurotransmitter stops.
      - the lack of glutamate results in depolarisation of the bipolar cell with which the rod synapses.
      - the neurone that make up the optic nerve are also depolarised and respond by producing an action potential
55
Q

types of brain scanning (4)

A
  1. MRI magnetic resonance imaging. scans use a magnetic field and radio waves to make images of soft tissues like the brain. MRI scans can be used to diagnose tumours, strokes, brain injuries and infections, and to track degenerative diseases like Alzheimers
  2. CAT. computerised axial tomography. scans use thousands of narrow beam X rays rotated around the patient. they only capture one moment in time and use harmful X-rays
  3. PET. positron emission tomography. scans use isotopes with short half lives, such as carbon 11 in glucose and other molecules. these act as radiotracers which are injected. they are detected on positron emission. increased blood flow to active area of the brain show up as bright spot on the scan. PET is useful in diagnosis and monitoring of Alzheimer’s
  4. fMRI. functional magnetic resonance. modified MRI technique detects activity in the brain following the uptake of oxygen in active brain areas. so it allows you to see the brain in action during live tasks.
56
Q

what happens during the critical period

A

columns in visual cortex narrower if they do not receive light.
axons compete for target cells in visual cortex. every time a neurone fires onto target cell other synapses weakened. axons that are not used are cut back.
1. there is a lack of visual stimulation in one eye
2. axons from the visually deprived eye do not pass impulses to cells in the visual cortex
3. axons from non deprived eye pass impulses to cells in visual cortex
4. inactive synapses are eliminated
5. synapses made by active axons are strengthened.

57
Q
  1. depth perception close objects

2. depth perception distant objects

A
  1. less than 30 m away
    we depend on the presence of cells that obtain information from both eyes at once
    the visual field is seen from 2 different angles and cells in the visual cortex let us compare the view from one eye with that from the other. stereoscopic vision and allows the relative position of objects to be perceived.
  2. for objects more than 30 m away the images on both retina’s are very similar. this means that visual cues and past experiences is used to interpret the image
58
Q

what happens in habituation

A
  1. with repeated stimulation, Ca2+ channels become less responsive so less Ca2+ crosses the presynaptic membrane
  2. less neurotransmitter is released
  3. there is less depolarisation of the postsynaptic membrane so no action potential is triggered in the motor neurone.
59
Q

what causes Parkinson’s disease

A

dopamine a neurotransmitter secreted by neurones including those located in the mid-brain. the axons of which extend throughout the frontal cortex, the brain stem and spinal cord.
dopamine secreting neurones in the basal ganglia die. these neurones normally release dopamine in the motor cortex. the motor cortex receives little dopamine and there is a lost of control of muscular movements.

60
Q

treatment for Parkinson’s disease (5)

A
  • slowing the loss of dopamine in the brain. MAO inhibitors which inhibits mono-amine oxidase, the enzyme responsible for the breakdown of dopamine. thereby increasing availability of dopamine. MAOA and MAOB.
  • treating symptoms with drugs. dopamine cannot be given as it cant cross the blood-brain barrier. L-dopa a precursor to dopamine can cross the barrier where it is converted into dopamine increasing concentration. main therapy.
  • dopamine agonists. are drugs that activate dopamine receptors directly and often more than one is gived. drugs mimic role of dopamine binding to receptors and triggering action potentials. they avoid high dopamine levels which has side effects.
  • gene therapy. trials in animals and phase 1 in humans show promise. genes for proteins that increase dopamine production, and that promote the growth and survival of nerve cells inserted into the brains.
  • deep brain stimulation (DBS) is a type of surgery used to treat symptoms of the disease. reduce medication reducing side effects
61
Q

effect of ecstasy (MDMA) affects synapses

A

MDMA increases the concentration of serotonin in the synaptic cleft. by binding to molecules in the presynaptic membrane that are responsible for transporting serotonin back into the cytoplasm. this prevents the removal from the synaptic cleft. drug may also cause the transporting molecules to work in reverse, further increasing amount of serotonin outside cell. high levels bring about mood changes. MDMA may have similar effect on molecules that transport dopamine as well.

62
Q

genetically modifying microorganisms

A
  • bacteria contain simple DNA structures, plasmids which can be transferred from one cell to another.
  • using restriction enzymes, the circular plasmids can be cut and using another set of enzymes a piece of DNA from another species can be inserted into it.
    The plasmid is inserted back into the bacteria, which are then allowed to multiply.
  • the protein produced is extracted from the culture
63
Q

genetic modification in plants

A
  • removal of plasmid from bacterial cell. plasmid is then cut with restriction enzyme.
  • identified gene of interest, the foreign gene is cut with the same restriction enzyme and inserted into the DNA plasmid along with a selected antibiotic marker
  • the plasmid is then reinserted into the bacterium. the bacterium is now allowed to introduce a plasmid vector with foreign DNA into plant cell. the foreign gene is the incorporated into the plant chromosome transforming the plant cell
  • alternatively after the DNA is inserted into the plasmid, it is coated with gold or tungsten and a gene gun is used to fire pellets coated in DNA into the plant cell at high velocity
  • the plate cells then put on a growth medium with antibiotic, only transformed cells will be selected
  • micropropagation: transformed cells grow in sterile culture medium containing sucrose, amino acids, inorganic ions and plant growth substances.
64
Q

what are the health concerns of GM plants

A
  • transfer of antibiotic resistance genes to microbes
  • formation of harmful products by new genes
  • transfer of viruses from animals to humans
65
Q

GM plants. environmental issues (3)

A
  • transfer of genes to non target species
  • possible breeding of superweeds
  • the possibility that GM crops will lead to the increased use of chemicals in agriculture.

Biology (13 decks)

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