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A-Level Biology > Unit 6 - Response to Stimuli > Flashcards

Unit 6 - Response to Stimuli Flashcards

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1
Q

what changes in their environment do organisms respond to & what is the effect?

A

organisms detect & respond to internal & external stimuli

–> increases survival chances & increases chances of reproduction so passes on beneficial alleles

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2
Q

why is there always a strong selection pressure?

A

to avoid danger/predation
to detect prey
to avoid toxic build up e.g. CO2
to ensure effective O2 delivery by altering heart rate

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3
Q

what is the purpose of taxis & kinesis?

A

they are simple movements that can maintain a mobile organism in a favourable environment

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4
Q

describe kinesis

A

simple, non-directional movement of mobile organism
in response to unfavourable stimulus
changes the speed at which the organism moves & the rate at which it changes direction depending on conditions
in response to non-directional stimulus e.g. temperature

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5
Q

in kinesis, what happens if an organism is in favourable conditions (or has just moved from favourable to unfavourable conditions)?

A

rate of changing direction increases to increase chances of returning to favourable conditions quickly

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6
Q

in kinesis, what happens if an organism is in unfavourable conditions?

A

rate of changing direction decreases so organism moves in straighter line to increase chances of finding a location with favourable conditions (surrounded by +ve stimuli)

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7
Q

describe taxis

A

more advanced than kinesis
directional movement of mobile organism towards favourable conditions & away from unfavourable conditions
+ve taxis = towards stimulus
-ve taxis = away from stimulus
in response to directional stimulus e.g. light, chemicals, gravity etc.

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8
Q

describe tropism & example

A

plant growth response (or part of a plant)
in response to directional stimulus
enable favourable conditions for max. growth

e.g. shoots show +ve phototropism & -ve gravitropism
roots show -ve phototropism & +ve gravitropism & +ve hydrotropism

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9
Q

what causes tropism?

A

uneven distribution of IAA auxin, which causes uneven cell elongation & growth

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10
Q

what do plants produce to control growth & responses to light & gravity?

A

hormones

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11
Q

what is the benefit of phototropism?

A

to aid photosynthesis

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12
Q

what is the benefit of gravitropism?

A

to obtain water, mineral ions & better anchorage

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13
Q

what does IAA stand for?

A

indolacetic acid

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14
Q

describe the response of shoots to light from directly above? (phototropism)

A

IAA diffuses evenly to both sides of the shoot
so even cell elongation & growth on both sides
so shoot grows straight up

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15
Q

describe the response of shoots to light from one direction? (phototropism)

A

IAA diffuses to shaded side of the shoot
so cells on shaded side elongate more & grow faster than cells on sunny side
so shoot grows towards light

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16
Q

what is the effect of the force of gravity on IAA?

A

the force of gravity causes IAA to accumulate on the underside of roots & shoots

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17
Q

describe gravitropism (response to gravity) in roots

A
  1. cells in root tip produce IAA
  2. IAA diffuses & accumulates on underside of root due to the force of gravity
  3. IAA inhibits cell growth & elongation on underside of root
  4. so cells on upperside grow faster & elongate more than underside cells
    –> so roots grow downwards in the direction of gravity
    +vely gravitropic
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18
Q

describe gravitropism (response to gravity) in shoots

A
  1. cells in shoot tip produce IAA
  2. IAA diffuses & accumulates on underside of shoot due to force of gravity
  3. IAA stimulates cell growth & elongation on underside of shoot
  4. so underside cells grow faster & elongate more than upperside cells
    –> shoot grows upwards against gravity
    -vely gravitropic
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19
Q

describe the organisation of the nervous system

A

CNS: brain, spinal cord

peripheral nervous system (PNS):
sensory pathways (S neurones from receptor to CNS)

motor pathways:
somatic/voluntary NS - conscious control e.g. movement
autonomic/involuntary NS - subconscious control e.g. heart rate: sympathetic - stimulate effectors & speed up
parasympathetic - inhibits effectors & slows down

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20
Q

what is a reflex & e.g.?

A

a rapid, short-lived, localised & involuntary response to a dangerous/harmful stimulus

e.g. removing hand from hot object

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21
Q

what makes a reflex rapid?

A

very few synapses (chemical message is slower than electrical impulse)
short neurone pathway
does not go to conscious part of brain

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22
Q

why are reflexes important? classic exam Q

A

to decrease or avoid damage - give e.g. related to Q
to escape from predators
to maintain balance/posture
role in homeostasis

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23
Q

describe the reflex arc (in exam, relate to Q)

A
  1. stimulus e.g. sharp pin
  2. receptor - pressure/mechanoreceptors in skin detect stimulus & generate potential in sensory neurone
  3. sensory neurone transmits action potential to spinal cord in CNS
  4. relay/intermediate neurone links sensory neurone to motor neurone
  5. motor neurone transmits action potential from spinal cord (CNS) to effector = muscle or gland e.g. muscles on finger/arm
  6. effector - muscle contracts/gland secretes e.g. finger/arm muscle contracts
  7. response e.g. pull finger/hand away from sharp object
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24
Q

from Seneca: function of dendrites, axon & cell body

A

dendrites carry impulse towards cell body
axon - away
cell body - where nucleus is located

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25
Q

what is the structure of a myelinated motor neurone?

A

one long axon

many dendrites - large SA for receiving action potentials (APs) from relay neurone

cell body - contains organelles, lots of RER & mitochondria for protein synthesis (channel proteins) & neurotransmitters

Schwann cells - wrap around axon, provide protection & electrical insulation & contains myelin sheath

nodes of Ranvier - gaps b/w Schwann cells where there is no myelin sheath

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26
Q

what are 3 functions of Schwann cells?

A

electrical insulation
phagocytosis
nerve regeneration

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27
Q

how does an AP travel along a neurone? (general structure)

A

by saltatory conduction
from one node of Ranvier to the adjacent node

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28
Q

what makes neurones excitable?

A

have resting potential & 3 protein transporters:
1. sodium-potassium pump
works all the time
all over the neurone

  1. open Na+ & K+ channels all over the neurone
    there are more K+ channels than Na+ channels - membrane is more permeable to K+
  2. voltage-gated channels
    sensitive to charge around them
    all over axon
    lots on axon hillock (mainly VgNa+)
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29
Q

describe the neurone when it has no membrane potential (theoretical)

A
  1. equal conc. K+ & Na+ inside & outside of axon
    no membrane potential: 0mV
    no diffusion of K+ & Na+
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30
Q

describe the neurone when decreasing membrane potential

A

sodium-potassium pump uses active transport to move 3 Na+ out & 2K+ into axon
–> increase conc. K+ & decrease conc. Na+ in axon
no K+ & Na+ diffusion

so overall decrease in # of positively charged ions in membrane –> decrease in membrane potential: -10mV

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31
Q

describe the neurone when creating & maintaining a resting membrane potential

A

sodium-potassium pump uses active transport to move 3 Na+ out & 2K+ into axon

K+ diffuses out of axon by fac. dif. via open channel proteins down electrochemical gradient

Na+ diffuses into axon by fac. dif. down electrochemical gradient

axon membrane is more permeable to K+ than Na+ so conc. of positive ions inside axon decreases to -65mV = resting potential

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32
Q

what are the essential factors for creating & maintaining resting potential?

A
  1. sodium-potassium pump actively transports 3Na+ out & 2K+ into axon using ATP
  2. axon membrane is more permeable to K+ (bc it has more K+ channel proteins) so more K+ diffuses out of axon than Na+ diffuses in
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33
Q

how is resting potential established (2 marker)?

A
  1. membrane is more permeable to K+ than Na+ bc it has more K+ channels
  2. sodium-potassium pump actively transports 3Na+ out & 2K+ into axon
    establishes electrochemical gradient
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34
Q

what is a generator potential?

A

a small depolarisation of the neurone’s membrane potential, causing a deviation from the resting potential at -65mV

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35
Q

define depolarisation

A

the neurone’s membrane becomes less negative due to an influx of Na+ ions

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36
Q

where do generator potentials occur?

A

at receptor cells or sensory nerve endings e.g. in Pacinian corpuscle

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37
Q

what causes generator potentials?

A

energy transduction, where a receptor detects a stimulus in an energy form (as a result of an energy change)
this energy is used to open VgNa+

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38
Q

how is an AP caused (linked to generator potentials)?

A

if generator potential causes a large enough depolarisation of membrane (above -50mV) due to sufficient diffusion of Na+ into axon, AP triggered

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39
Q

what is the all or nothing law?

A

any stimulus that causes the membrane potential to reach/exceed the threshold value triggers an AP

all APs have the same magnitude

generator potentials below the threshold value of -50mV will not trigger an AP

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40
Q

describe the movement of Na+ ions when the stimulus is sub-threshold

A
  1. receptor detects a small energy change/stimulus
  2. some Vg Na+ channels open –> some Na+ diffuses into axon, down electrochemical gradient by fac. dif. –> membrane potential slightly less negative but does not reach threshold value of -50mV
  3. other VgNa+ channels do NOT open so no AP triggered
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41
Q

describe the movement of Na+ ions when the stimulus is above threshold

A
  1. receptor detects large energy change/stimulus
  2. many VgNa+ channels open –> lots of Na+ ions diffuse into axon down EC gradient –> large depolarisation of membrane
  3. this causes positive feedback = more VgNa+ channels to open –> greater influx of Na+ –> this reaches/exceeds the threshold value of -50mV so AP is triggered
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42
Q

all APs are the same amplitude no matter how large the initiating stimulus

A
43
Q

what are the stages of the action potential?

A

resting potential
depolarisation
repolarisation
hyperpolarisation
restoring resting potential

44
Q

what happens during resting potential?

A

-65 mV
sodium-potassium pump moving 3Na+ ions out & 2K+ ions into axon
VgNa+ & VgK+ channels closed

45
Q

what happens during depolarisation?

A

generator potential up to -50mV
fac. diff. Na+ ions into cell down electrochemical gradient
membrane potential becomes more positive
at -50mV threshold, Vg Na+ channels open, causing influx of Na+
this causes positive feedback so more Na+ channels open
membrane potential increases to +40mV

46
Q

what happens at +40mV?

A

Na+ equilibrium is reached at +40mV
VgNa+ channels close & VgK+ channels open

47
Q

what happens during repolarisation?

A

VgNa+ channels close & VgK+ channels open
fac. diff. of K+ ions out of axon down electrochemical gradient
membrane potential becomes more -ve

48
Q

what happens during hyperpolarisation?

A

when K+ ions diffuse out, membrane potential becomes more -ve than resting potential (as VgK+ channels are slow to close)
VgNa+ & VgK+ channels close
K+ equilibrium is reached at-90mV

49
Q

what is the importance of the refractory period?

A

no AP can be generated in hyperpolarised parts of membrane
promotes separate impulses
ensures unidirectional impulse
creates a time delay b/w APs
limits frequency of AP

50
Q

describe the passage of AP in an unmyelinated axon

A
  1. stimulus causes influx of Na+ ions so first section of membrane depolarises
  2. localised currents occur
  3. which causes VgNa+ channels further along membrane to open so neighbouring regions of membrane depolarise
  4. meanwhile, the previous region of membrane repolarises & is hyperpolarised then resting potential restored
51
Q

describe the passage of AP in a myelinated axon

A

axon surrounded by myelin sheath produced by Schwann cells wrapping around axon
myelin is a mixture of lipids & acts as insulation
there are not VgNa+ or VgK+ channels in the axon membrane underneath the myelin
APs can only happen at Nodes of Ranvier, which are gaps b/w the myelin sheath
localised currents stretch b/w Nodes of Ranvier, speeding up the transmission of the impulse by 3 times
the impulse jumps b/w Nodes of Ranvier, which is saltatory conductance

52
Q

what factors affect the speed of conductance of AP?

A

the myelin sheath
axon diameter
temperature

53
Q

how does the myelin sheath affect the speed of conductance?

A

causes nerve impulses to jump from one Node of Ranvier to another, called saltatory conduction
this increases the speed of transmission

54
Q

how does the diameter of the axon affect the speed of conductance?

A

the greater the diameter, the faster the speed of impulse
bc less leakage of ions from larger axons
so easier to maintain membrane potential

55
Q

how does temperature affect the speed of conductance?

A

the higher the temperature, the faster the speed of impulse up to a point
increased temp. = increased rate of diffusion of Na+ & K+ ions bc increased KE
increased temp. = increased rate respiration so increased atp production for sodium-potassium pump

56
Q

greater strength of stimulus

A

= greater frequency of APs

57
Q

what is the function of a synapse?

A

electrical impulse cannot travel over junction b/w neurones
neurotransmitters send impulses b/w neurones & to effectors
new impulses can be initiated in several different neurones for simultaneous responses

58
Q

define synapse

A

the gap b/w 2 neurones
the point where one neurone communicates with another neurone or w an effector

59
Q

describe the structure of a cholinergic synapse

A

presynaptic neurone:
presynaptic knob:
lots of mitochondria
SER
VgCa2+ ion channels
synaptic vesicles containing neurotransmitter/acetylecholine (ACh)

synaptic cleft:
gap b/w neurones

postsynaptic neurone:
receptors complementary to neurotransmitter/ACh
ligand-gated Na+ channels

60
Q

how does an impulse travel across a cholinergic synapse?

A
  1. When AP arrives, Na+ enters through VgNa+ channel. depolarisation of membrane causes VgCa2+ channels to open.
  2. Ca2+ ions enter via fac. dif., causing vesicles containing ACh to move towards presynaptic membrane (requires ATP)
  3. vesicles fuse with presynaptic membrane & release ACh into synaptic cleft (exocytosis)
  4. ACh diffuses across synaptic cleft towards post-synaptic membrane
  5. ACh binds to complementary receptors on ligand-gated Na+ channels on post-synaptic membrane. ligand-gated Na+ channels open so Na+ diffuses in
  6. this causes depolarisation of post-synaptic membrane so VgNa+ channels open so Na+ diffuses into axon so new AP initiated
61
Q

how does a synapse ensure unidirectionality of impulse?

A

1- neurotransmitter only produced in presynaptic neurone

2- ligand-gated Na+ channels are only in post-synaptic membrane

so impulse always goes from presynaptic to postsynaptic neurone

62
Q

what happens when ACh binds to ligand-gated Na+ channels?

A

ACh binds to receptor site
which causes conformational change in protein (3 structure changes)
so Na+ enters

63
Q

why is ACh recycled?

A

too slow & energy costly to produce new ACh every time

64
Q

describe how neurotransmitter/ACh is recycled

A
  1. enzyme acetylcholinesterase (AChE) binds to ACh & hydrolyses ACh into acetyl + choline so it is released from receptors & ligand-gated Na+ channels close

prevents overstimulation of skeletal muscle cells

  1. choline is reabsorbed into presynaptic knob & recombined with acetyl in SER (requires ATP)
  2. ACh is packaged into vesicles for future use
65
Q

define summation & name the 2 types

A

neurotransmitter from several sub-threshold impulses accumulate to generate an AP

temporal summation
spatial summation

66
Q

define & describe the process of spatial summation

A

several simultaneous APs from different presynaptic neurones cause neurotransmitter release & converge onto one postsynaptic neurone

sub-threshold: if AP from only one presynaptic neurone, insufficient neurotransmitter is released

above threshold: if AP from more than one presynaptic neurone, sufficient neurotransmitter is released so AP triggered in postsynaptic neurone

67
Q

define & describe the process of temporal summation

A

one presynaptic neurone has a high frequency of APs so releases neurotransmitter several times quickly

sub-threshold: no AP in postsynaptic neurone bc insufficient neurotransmitter released

above threshold: AP produced in postsynaptic neurone bc sufficient neurotransmitter released

68
Q

what type of synapse is a cholinergic synapse?

A

excitatory

69
Q

describe excitatory synapse

A

AP in presynaptic neurone increases chance of AP occurring in postsynaptic neurone

70
Q

describe inhibitory synapse

A

AP in presynaptic neurone decreases the chance of AP occurring in postsynaptic neurone
1. neurotransmitter binds to & opens Cl- channels in postsynaptic membrane & K+ channels open
2. Cl- moves in & K+ moves out by fac. dif.
3. membrane potential becomes more -ve = hyperpolarised
4. reaching -50mV threshold for AP is less likely bc more excitatory neurotransmitter is needed

71
Q

by what mechanisms do drugs increase & decrease synaptic transmission?

A

increase: inhibit AChE
mimic shape of neurotransmitter & bind to receptor site on ligand-gated Na+ channel so it opens

decrease: inhibit release of NT
decrease permeability of postsynaptic neurone to ions
hyperpolarise postsynpatic membrane

72
Q

what is the function of receptors?

A

cells that detect stimuli (changes in the internal & external environment)

73
Q

each receptor responds to…
thermo-
photo-
mechano-
chemo-

A

a different & specific type of stimulus
thermo- detect heat energy only
photo- detect light energy only
mechano- detect pressure only
chemo- detect chemicals only

74
Q

define sensory reception & sensory perception

A

sensory reception: the function of receptors (receiving info.)
sensory perception: making sense of info. from receptors (interpretation) (largely the function of the brain)

75
Q

describe 2 important features of receptors e.g. Pacinian corpuscle

A
  1. specific to a single type of stimulus: e.g. mechanical pressure only
  2. produces a generator potential by acting as a transducer
    all stimuli involve change in energy
    transducer/receptor converts this energy change into electrical nerve impulse/generator potential –> AP
    e.g. PC transduces mechanical energy of stimulus into generator potential –> AP
76
Q

where are PCs located?

A

deep in skin
lots in fingers & soles of feet
joints, ligaments & tendons where they allow organism to know which joints are changing direction (proprioperception)

77
Q

what is the structure of PC?

A

see diagram
lamellae
capsule
blood capillary
sensory neurone ending
axon of sensory neurone
stretch-mediated Na+ channels
direction of AP

78
Q

what are the lamellae of a PC?

A

layers of connective tissue with gel b/w them

79
Q

how does the PC transduce mechanical energy into GP?

A

sensory neurone ending at centre of PC has stretch-mediated Na+ channels in CSM
when PC is deformed, the channels’ permeability to Na+ increases

80
Q

describe the PC at resting state

A

the stretch-mediated Na+ channels are too narrow to allow Na+ to diffuse into the axon
PC has resting potential at -65mV

81
Q

describe the process by which the PC causes an AP

A

when pressure is applied to the PC
lamellae are deformed & membrane around sensory neurone is stretched
this widens the stretch-mediated Na+ channels & Na+ diffuses into the axon of the sensory neurone
membrane depolarises & produces a GP
GP turns into AP if threshold value (-50mV) reached, which travels to CNS

82
Q

what is the function of:
retina
fovea
blind spot
optic nerve?

A

retina: contains photoreceptors (rods & cones) & transmits APs to optic nerve
fovea: only cones, area of highest visual acuity
blind spot: no photoreceptors so light that falls on this spot is not perceived - exit of ganglion neurones of the optic nerve
optic nerve: transmits impulses generated in retina to cerebral cortex

83
Q

what are the visual pigments of rods & cones?

A

rods: rhodopsin
cones: there are 3 different type of cone cells each with a different variant of iodopsin

84
Q

what is the colour perception of rods & cones?

A

rods: monochromatic (black & white)
cones: trichromatic (blue, green & red bc of different iodopsin variants)

85
Q

how many rods & cones are there in each eye?

A

120 million rods
6 million cones

86
Q

what is the distribution of rods & cones?

A

rods: all over retina but not in fovea
exclusively rod cells in periphery of retina

cones: all over retina but greatest density at fovea
no cones at periphery

87
Q

define visual acuity

A

clarity - ability to distinguish b/w 2 points close together

88
Q

describe the visual acuity of rods

A

lower visual acuity
many rod cells converge onto one bipolar neurone = spatial summation = retinal convergence
2 points of light falling on retina are seen as one point bc only one AP sent

89
Q

describe the visual acuity of cones

A

higher visual acuity
one cone cell joins to one bipolar neurone
2 points of light perceived as 2 distinct points

90
Q

rod/cone –> bipolar neurone –>

A

ganglion neurone

91
Q

describe rod cells’ sensitivity to light

A

more sensitive to light
bc rhodopsin breaks down more easily –> AP

also spatial summation effect of retinal convergence
/sufficient neurotransmitter released
= more likely to reach threshold value & trigger AP

92
Q

describe cone cells’ sensitivity to light

A

less sensitive to light
as iodopsin breaks down less easily
to require higher light intensity to cause AP
also no retinal convergence

93
Q

benefit to mammals of having different photoreceptor cells?

A

good all-round vision day & night

94
Q

what is the autonomic nervous system & what 2 parts does it consist of?

A

part of the peripheral nervous system that controls involuntary processes

  1. parasympathetic nervous system - inhibits effectors –> slows down processes inc. decreases heart rate
  2. sympathetic nervous system - stimulates effectors –> speeds up processes inc. increases heart rate
95
Q

describe cardiac muscle

A

makes up heart walls
myogenic - contraction is initiated from within itself (SAN) rather than from external impulses (like with skeletal muscles)

96
Q

label diagram of the heart

A

see booklet

97
Q

what is the cardiac cycle initiated by?

A

small area of cardiac muscle called the SAN/pacemaker which sets the rhythm for all other cardiac muscle ~65bpm resting hr

98
Q

describe the sequence of events that control basic heart rate

A
  1. SAN send excitation wave of electrical activity over the atrial walls
  2. both atria contract
  3. the atrioventricular septum is non-conductive tissue that causes a delay b/w atrial & ventricular contraction
    –> this allows atria to empty/ventricles to fill with blood fully
  4. wave is conducted through the AVN
  5. AVN causes short delay before passing on the wave to Purkyne fibres that make up the Bundle of His
  6. the wave of electrical activity is transmitted to the apex the spreads upwards
  7. both ventricles contract from the apex upwards, pumping blood out the heart
99
Q

what stimuli cause an increase in heart rate?

A

exercise (increased CO2)
stress/fear
low blood pressure

100
Q

what are the functions chemo- & baro- receptors & where are they located?

A

chemoreceptors detect changes in pH
increased CO2 = decreased pH

baroreceptors detect stretch/pressure in blood vessels

both found in lining of blood vessels e.g. aorta & carotid arteries

101
Q

what stimuli cause a decrease in heart rate?

A

recovery (decreased CO2)
rest
high blood pressure

102
Q

how is heart rate increased?

A
  1. stimulus (specific to Q) is detected by receptors (specific to Q - chemo- detect increase in CO2 = decrease in pH or baro- detect stretch/pressure in blood vessels) in lining of blood vessels
  2. receptors send impulses to cardiac acceleratory centre in medulla
  3. more impulses are sent via sympathetic neurones e.g. cardiac nerve
  4. to the SAN
  5. then noradrenaline is released at an excitatory synapse
  6. this increases frequency of impulses to AVN

rate & force of contraction increases
cardiac output increases
blood pressure increases

103
Q

what is the effect of increased cardiac output?

A

CO = HR X stroke volume (volume of blood pumped out the heart per beat)

more CO2 removed & more O2 delivered from muscles

104
Q

how is heart rate decreased?

A
  1. stimulus (specific to Q) is detected by receptors (specific to Q - chemo- detect increase in CO2 = increase in pH or baro- detect stretch/pressure in blood vessels) in lining of blood vessels
  2. receptors send impulses to cardiac inhibitory centre in medulla
  3. more impulses are sent via parasympathetic neurones e.g. vagus nerve
  4. to the SAN
  5. then acetylcholine is released at an inhibitory synapse –> K+ channels open, causing hyperpolarisation of post-synaptic membrane
  6. this decreases frequency of impulses to AVN

rate & force of contraction decreases
cardiac output decreases
blood pressure decreases

A-Level Biology (10 decks)

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