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Cell biology semester 1 > excitable cells > Flashcards

excitable cells Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

action potential

A

rapid change in membrane potential
from -70 to 60 mV

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2
Q

how is the resting membrane potential maintained?

A

high permeability to K+
active transport of Na+ across membrane
transmembrane proteins (K+ leak channel and Na+ pump)

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3
Q

electrogenic

A

creating slight positive charge outside of cell

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4
Q

equilibrium potential

A

voltage at which the electrical gradient is equal and opposite to that of K+ concentration gradient
K+ therefore stops moving

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5
Q

how is equilibrium potential determined?

A

the nernst equation

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6
Q

nernst equation

A

(-RT/zF)Ln (conc (ion in)/conc(ion out))

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7
Q

equilibrium potential of K+

A

-86 mV

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8
Q

equilibrium potential of Na

A

+60mV

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9
Q

equilibrium potential of Cl

A

-70mV

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10
Q

resting membrane potential

A

-70mV

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11
Q

what equation determines resting membrane potential?

A

the Goldmann equation

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12
Q

why is RMP closer to Ek than ENa?

A

biggest weighting given to most permeable ion

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13
Q

V-gated Na+ channel

A

potential reaches -55mV
Na+ rushes through activation gate of channel

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14
Q

sodium activation gate

A

voltage and time dependent

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15
Q

sodium inactivation gate

A

time-dependent

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16
Q

sodium gate open to inactivated

A

fast and automatic

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17
Q

sodium gate inactivated to closed

A

slow automatic

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18
Q

sodium gate closed to open

A

fast
voltage-gated

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19
Q

voltage gated K+ channel

A

opens at membrane depolarisation slower than Na+
closes slowly in response to repolarisation

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20
Q

K+ gate open to closed

A

slow
voltage-gated

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21
Q

K+ closed to open

A

slow
voltage gated

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22
Q

absolute refractory period

A

period in which membrane can’t generate another action potential despite stimulus size.
sodium channels are inactivated

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23
Q

relative refractory period

A

period in which membrane can generate another a.p, only if stimulus is bigger than normal
some Na+ recovered
some K+ still open

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24
Q

where does a.p start

A

axon hillock

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25
Q

refractory period function

A

prevents a.p. being set off backwards

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26
Q

velocity of action potential

A

proportional to sqrt (diameter*membrane resistance)

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27
Q

consequence of diameter on neuron transmission

A

more room for local current flow in loops

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28
Q

consequence of resistance on neuron transmission

A

lower resistance = less current lost by leaking

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29
Q

what affects a.p velocity in a myelinated neuron

A

resistance
diameter
distance between nodes of ranvier

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30
Q

multiple sclerosis

A

demyelinating disorder causing gradual loss of motor function
a.p. unable to jump between nodes of ranvier

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31
Q

what happens when a.p invades neuron terminal?

A

membrane is depolarised and voltage-gated calcium ion channels open

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32
Q

what happens when voltage-gated calcium ion channels open?

A

Ca2+ rushes into axon terminal, causing vesicle fusion with the presynaptic membrane

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33
Q

what happens when vesicles fuse to the pre-synaptic membrane?

A

vesicles release ACh into the synaptic cleft so that they diffuse across and bind to postsynaptic receptors

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34
Q

what happens when ACh binds to post-synaptic receptors?

A

ligand-gated Na+ channels open and rush into postsynaptic cell and K+ out, reaching endplate potential of -15mV

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35
Q

endplate potential

A

1/2 total equilibrium potentials of sodium and potassium ions

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36
Q

a.p at junction folds

A

none as there’s no voltage-gated Na+ channels

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37
Q

what happens when EPP reaches -15mV?

A

EPPs in junctional folds trigger a.p’s nearby, propagating deep to trigger contraction

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38
Q

smallest EPP generated
when

A

0.5mV
occurs at random when nerve is at rest

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39
Q

1mEPP

A

1 vesicle fusion =1 quantum=10000ACh

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40
Q

1EPP

A

100mEPP therefore 100 vesicles

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41
Q

safety factor of neurones

A

margin of 200-300 vesicle releases for normal a.p at NMJ

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42
Q

what does acetylcholine break down into?

A

choline + acetate
reforms via acetyl coA

43
Q

acetylcholinesterase location

A

junctional folds in the synaptic cleft

44
Q

acetylcholinesterase function

A

cleaves ACh so action potentials aren’t transient

45
Q

curare

A

South American arrow poison causing paralysis by blocking ACh receptor
also used as muscle relaxant by anaesthetists

46
Q

botulinum toxin

A

inhibits exocytosis so ACh release is blocked
used in botox
bacteria in tinned food

47
Q

myasthenia gravis

A

autoimmune disorder
antibodies destroy ACh receptors
safety factor means many antibodies need to accumulate for NMJ to stop functioning
treated by ACh-ase inhibitors

48
Q

sarcoplasmic reticulum

A

protein pumps transport Ca2+ ions into T-tubules

49
Q

T-tubules

A

deep infoldings in sarcolemma
get a.p. into parts of muscle that membrane can’t reach

50
Q

muscle fibre size

A

roughly 100micrometers

51
Q

what happens during muscle contraction to muscle

A

shortens
myosin/ actin don’t change length
actin slides over myosin (thick)

52
Q

Z-line

A

vertical line of actin

53
Q

M-line

A

vertical line of myosin

54
Q

H band
length change during contraction?

A

distance between actin filaments
shortens

55
Q

A band
length change during contraction?

A

length of myosin horizontal filaments
no change

56
Q

I band
length change during contraction?

A

distance between myosin filaments
shortens

57
Q

myosin

A

thick filament
fibrous protein with globular head
held together by M-line

58
Q

actin

A

thin filaments
globular protein (G-actin) linked to form chain
2 F-actin strands twist to form double helix

59
Q

tropomyosin

A

fibrous protein twisted around actin

60
Q

troponin

A

attached to actin at regular intervals

61
Q

3 sub-units of actin filament

A

T/I > tropomyosin and actin binding
C> Ca2+ binds to C, uncovering binding site

62
Q

G-actin number of binding sites

A

1

63
Q

sarcolemma

A

tubular structure surrounding myofibrils
enlarges into terminal cisternae
stores much Ca2+

64
Q

what happens when there’s an a.p in t-tubules?

A

triggers Ca2+ release from terminal cistae of sarcoplasmic reticulum, triggering contraction
Ca2+ binds to troponin-C, uncovering myosin binding site on actin to form cross-bridge

65
Q

excitogen contraction coupling

A
  1. myosin in high-energy state, hydrolysing ATP
  2. myosin heads rotate> powerstroke
  3. ATP binds to myosin head, breaking actin-myosin bond and releasing ADP+Pi
  4. ATP split returning myosin to high energy state
66
Q

number of myosin heads in one muscle fibre

A

500

67
Q

how many cycles per second in one muscle fibre

A

5

68
Q

muscle relaxation

A

SR removes Ca2+ via Ca-ATPase pump
ATP binds to myosin

69
Q

3 types of neurone

A

motor (efferent)
interneurone
sensory (afferent)

70
Q

where are interneurones located

A

CNS

71
Q

types of sensory neurone

A

pseudo-unipolar > somatic senses
bipolar> smell and vision

72
Q

neurone characteristics

A

don’t divide (foetal neurones lose mitosis ability)
longevity
high metabolic rate

73
Q

2 types of electrical signal in neurones

A

action potential
graded potential

74
Q

action potential characteristics

A

large, uniform depolarisations travelling rapidly for long distances w/o losing strength
all or none

75
Q

graded potentials

A

variable strength signals that travel over short distances, losing strength
can generate a.p’s

76
Q

where do graded potentials occur?

A

in dendrites, cell bodies or axon terminals
NOT AXONS

77
Q

depolarizing graded potential

A

excitatory post-synaptic potential
EPSP

78
Q

hyperpolarizing graded potential

A

inhibitory post-synaptic potential
IPSP

79
Q

threshold voltage

A

-55mV

80
Q

subthreshold vs suprathreshold

A

below / reachind threshold

81
Q

pros of frequency encoded signals

A

digital and therefore less prone to ‘noise’
greater fidelity

82
Q

divergence

A

presynaptic neurone branching to affect large number of postsynaptic neurones

83
Q

convergence

A

large number of presynaptic neurones converge to affect smaller number of postsynaptic neurones

84
Q

spatial summation

A

EPSP’s originating simultaneously at different locations on the neurone to form suprathreshold signal and therefore an a.p.

85
Q

postsynaptic inhibition

A

EPSP’s diminished by summation with an IPSP, meaning summed potential is subthreshold and therefore no a.p.

86
Q

temporal summation

A

summation occurring from graded potentials overlapping in time

87
Q

postsynaptic integration/ modulation

A

evaluation of strength / duration of signals to determine action potential firing

88
Q

presynaptic modulation characteristics

A

more precise
excitatory/ inhibitory

89
Q

presynaptic similarities

A

action potential
Ca2+ channel opening and Ca2+ increases in concentration to cause exocytosis
neurotransmitter diffuses across cleft

90
Q

postsynaptic differences

A

neurotransmitter identity
receptor identity and mechanisms

91
Q

neurotransmitter examples

A

ACh
amines
amino acids
polypeptides
purines
gases

92
Q

2 receptor mechanisms

A

ligand-gated ion channels (inotropic)
G-protein coupled receptors (metabotropic)

93
Q

inotropic channel characteristics
example

A

fast synaptic potential
e.g. nicotinic

94
Q

metabotropic channel characteristics
example

A

activates 2nd messenger systems
slow synaptic potential
e.g. muscarinic

95
Q

advantage of inotropic/ metabotropic receptors

A

adds diversity to the system

96
Q

synaptic plasticity

A

variation of electrical activity, causing rearrangmenets of circuit connections

97
Q

long-term potentiation

A

process by which repetitive stimulation at a synapse increases the efficacy of transmission at that synapse

98
Q

where was LTP first observed?

A

in the hippocampus

99
Q

how is LTP prevented?

A

by Ca2+ removal from extracellular medium

100
Q

main excitatory transmitter in CNS

A

glutamate

101
Q

LTP process

A

glutamate released and binds to NMDA and AMPA inotropic receptors.
repetitive stimulation results in greater depolarisation, Mg2+ ejected from NMDA receptor so Ca2+ can flow through.
therefore, postsynaptic cell more sensitive to glutamate release from presynaptic cell.

102
Q

AMPA

A

Na+ channel triggering EPSP

103
Q

NMDA

A

blocked by Mg2+ therefore no effect

Cell biology semester 1 (6 decks)

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