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bio > 3.6 Organisms respond to changes in enviroment > Flashcards

3.6 Organisms respond to changes in enviroment Flashcards

1
Q

define stimulus

A

change in internal/external environment

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2
Q

steps of a reflex arc

A

stimulus->receptor->sensory neurone->coordinator->CNS->relay neurone->motor neurone->effector ->response

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3
Q

why is a reflex arc important

A 
rapid 
-only 3 neurones 
autonomic 
-doesnt have to be learnt
protects from harmful stimuli
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4
Q

define taxis

A

directional respone

moves toward favourable stimulus

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5
Q

kinesis

A

non directional movement towards stimulus

change speed/movement in response to stimulus

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6
Q

how does IAA result in phototropism in shoot

A
  • cells in shoot tip produce IAA-> transported down shoot
  • IAA conc increases on shaded side
  • promotes cell elongation
  • shoot bends towards light
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7
Q

how does IAA result in gravitropism in roots

A
  • cells in shoot tip produce IAA-> transported down shoot
  • IAA conc increases on lower side of root
  • inhibits cell elongation
  • root curves downwards towards gravity
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8
Q

how does pacinian corpuscle respond

A

generating a generator potential

  • mechanical stimulus deforms lamellae + stretch mediated sodium ion channel
  • sodium ion channels open + sodium ions diffuse into sensory neurone
  • greater pressure causes more channels to opens + more sodium ions to enter
  • cause depolarisation
  • leading to generator potential
  • triggers action potential
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9
Q

rods summary

A
  • more at periphery of retina, absent in fovea
  • one type of rod, one type of pigment
  • one bipolar
  • very sensitive to light
  • low visual acuity
  • black + white vision
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10
Q

cones summary

A
  • concentrated at fovea, fewer at periphery of retina
  • 3 types of cones containing 3 pigments
  • one cone one neurone
  • less sensitive to light
  • high visual acuity
  • colour vision
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11
Q

why are rods more sensitive to light

A
  • rods conncected in groups to one bipolar
  • spatial summation
  • stimulation of each individual cell is subthreshold
  • so more likely to exceed/meet threshold + generate action potential
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12
Q

why are cones less sensitive to light

A
  • one cone joins to one neurone

- no spatial summation

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13
Q

why do cones have higher visual acuity

A
  • one cone to one neurone
  • brain receives seperate impulses
  • can distinguish between different sources of light
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14
Q

why do rods have lower visual acuity

A
  • rods connceted in groups to one bipolar cell
  • spatial summation
  • many neurones only one impulse
  • cant distinguish between seperate sources of light
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15
Q

why do cones allow colour vision

A
  • 3 types of cones
  • different pigments->absorb different wavelengths
  • stimulation of different combinations
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16
Q

describe the control of heart rate

A

SAN sends out regular electrical waves across both atria
-causing both atria to simultaneously contract
layer of nonconductive tissue prevents wave directly crossing to ventricles
waves of electrical activity reaches AVN, delays impulse, allows atria to fully contract + empty
AVN passes wave of electrical activity to bundle of His to apex of heart
-ventricles contract simultaneously from base upwards

17
Q

effect of baroreceptors

A

found in aorta + carotid artery
low bp
-more frequent impulses to medulla
-more frequent impulses to SAN along sympathetic neurones
-more impulses sent from SAN
-cardiac muscle contracts more frequently, heart rate increases

high bp

  • more frequent impulses to medulla
  • more frequent impulses sent to SAN via parasympathetic neurones
  • less frequent impulses from SAN
  • cardiac muscle contracts less frequently, heart rate decreases
18
Q

effect of chemoreceptors

A

found in aorta + carotid artery
low pH
-more frequent impulses to medulla
-more frequent impuleses to SAN via sympathetic neurones
-more frequent impulses from SAN
-cardiac muscle contracs more frequently, heart rate increases

high pH

  • more frequent impulses to medulla
  • more frequent impulses to SAN via parasympathetic neurones
  • less frequent impulses from SAN
  • cardiac muscle contracts less frequently, heart rate decreases
19
Q

describe the establishment of a resting potential

A
  • Na+/K+ pump actively transports 3 Na+ out axon 2 K+ in
  • electrochemical gradient
  • membrane more permeable to K+, K+ channels open , than Na+, Na+ channels closed
  • K+ move out axon by facilliated diffusion
  • inside axon relatively negative compared to outside
20
Q

generation of an action potential steps

A

stimulus

  • membrane more permeable to Na+ as Na+ channels open
  • Na+ diffuses into neurone via electrochemical gradient

Depolarisation

  • P.d reaches threshold, action potential generated
  • because more voltage gated Na+ channels open, Na+ diffuses in rapidly

Repolarisation

  • Na+ channels close (membrane less permeable)
  • voltage gated K+ channels open,
  • K+ difufuse out neurone

Hyperpolarisation
-K+ channels slow to close=slight overshoot

Resting potential restored
-by K+/Na+ pump

21
Q

what is the refractory period

A

time to restore axon to resting potential

22
Q

importance of refractory period

A
  • produces discrete + discontinuous impulses

- unidirectional action potential

23
Q

effect of myelination on speed of conductance

A
  • depolarisation at Nodes of Ranvier only ->saltatory conduction
  • impulse doesn’t travel whole axon
24
Q

effect of axon diameter on speed of conductance

A

bigger diameter means less leakage of ions

less resistance of flow to ions

25
effect of temperature on speed of conductance
- increases rate of movement of ions as more KE - higher rate of respiration->ATP produced faster + faster energy release->faster active transport - proteins can denature at certain temp
26
passage of an action potential in non myleinated axon
- action potential passes as wave of depolarisation - influx of Na+ in one region increases permeability of adjacent region to Na+ by causing - voltage gated Na+ channels to open - adjacent region depolarises
27
describe the transmission across a cholinergic synapse
- action potential arrives, Ca+ channels open -> Ca+ diffuses into presynaptic neurone - causing vesicles containing neurotransmitter to move towards + fuse with presynaptic membrane + release neurotransmitter into synaptic cleft via exocytosis - neurotransmitter diffuses across synaptic cleft-> bind to specific receptors found only on post synaptic membrane - Na+ channels open-> Na+ diffuses into post synaptic knob->depolarisation initiates action potential - neurotransmitter removed from cleft so response doesn't keep happening - products reabsorbed by presynaptic neurone
28
cholinergic synapse vs neuromuscular junction
cholinergic- neurone to neurone/ neuromuscular - neurone to muscle neuromuscular- always excitatory, always triggers action potential neuromuscular- post synpatic memb has more receptors than other synapses neuromuscular-lots of fold on post synaptic memb which forms clefts to store enzyme to break down neurotransmitter
29
why do synapses result in unidirectional nerve impulses
- neurotransmitter made in presynaptic neurone | - receptors only on post synaptic membrane
30
describe spatial summation
many presynaptic neurones share same post synaptic neurone collectively release sufficient neurotransmitter to reach threshold to trigger action potential
31
describe temporal summation
one presynaptic neurone releases neurotransmitter many times over short period sufficient neurotransmitter to reach threshold to trigger action potential
32
how does inhibition by inhibitory synapses work
they hyperpolarise postsynaptic membrane -K+ channels open, K+ diffuses out -Cl- channels open, Cl- diffuse in inhibits formation of action potential -cant be depolarised -reduced effect of Na+ entering so less likely to reach threshold
33
how do muscles work
as antagonistic pairs - one muscle contracts -> produces force - one muscle contracts
34
what does a sarcomere consist of
``` ends - Z line Middle - M line H zone- only myosin A band -myosin + actin I bond - only actin ```
35
what happens to the sarcomere during muscle contraction
myosin head slides past actin, causing sarcomere to contract | -H zone shorter, I band shorter, A band same, Z line closer
36
describe the sliding filament theory of muscle contraction
1. action potential spreads down T tubules causing release of Ca2+ from sarcoplasmic reticulum, which diffuse through sarcoplasm to myofibril 2. Ca2+ bind to tropomyosin, causing it to move as it changes shape, exposing actin myosin binding site 3. myosin head attach to binding site forming actinmyosin crossbridge, requires ATP 4. myosin heads move forward(power stroke) pulling actin along myosin 5. ATP binds to myosin head, breaking crossbridge 6. hydrolysis of ATP causes myosin heads to move back to original position 6. myosin reattaches to different binding site further along actin
37
features of slow twitch fibres
- specialised for slow, sustained contractions - endurance activities - in muscles that give posture - aerobic respiraton-->produces ATP, releases energy slowly-->store large amount of o2 for aerobic r - many mitochondria -->high rate of resp - many capillaries-->short diffusion pathway-->supply high conc of o2 for aerobic r + prevent lactic acid build up-->causing muscle fatigue
38
features of fast twitch fibres
- specialised for rapid, intense contractions - short burts of speed + power - anaerobic respiration-->produces ATP-->release energy quickly - low levels myoglobin->whitish colour->doesn't need lots of o2 - lots of glycogen->hydrolysed to lots of glucose->used during glycolysis, inefficient - high conc og enzymes - store phosphocreatine, rapidly generates ATP from ADP by providing phosphate - muscles can get fatigued quickly -> high amounts of lactate
39
roles of phosphocreatine in muscle creatine
- stored inside cells - rapidly makes ATP by phosphorylating ADP - PCr runs out after few seconds --> short bursts of vigorous exercise - anaerobic + alactic

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