excitable cells 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
refractory period function
prevents a.p. being set off backwards
26
velocity of action potential
proportional to sqrt (diameter*membrane resistance)
27
consequence of diameter on neuron transmission
more room for local current flow in loops
28
consequence of resistance on neuron transmission
lower resistance = less current lost by leaking
29
what affects a.p velocity in a myelinated neuron
resistance diameter distance between nodes of ranvier
30
multiple sclerosis
demyelinating disorder causing gradual loss of motor function a.p. unable to jump between nodes of ranvier
31
what happens when a.p invades neuron terminal?
membrane is depolarised and voltage-gated calcium ion channels open
32
what happens when voltage-gated calcium ion channels open?
Ca2+ rushes into axon terminal, causing vesicle fusion with the presynaptic membrane
33
what happens when vesicles fuse to the pre-synaptic membrane?
vesicles release ACh into the synaptic cleft so that they diffuse across and bind to postsynaptic receptors
34
what happens when ACh binds to post-synaptic receptors?
ligand-gated Na+ channels open and rush into postsynaptic cell and K+ out, reaching endplate potential of -15mV
35
endplate potential
1/2 total equilibrium potentials of sodium and potassium ions
36
a.p at junction folds
none as there's no voltage-gated Na+ channels
37
what happens when EPP reaches -15mV?
EPPs in junctional folds trigger a.p's nearby, propagating deep to trigger contraction
38
smallest EPP generated when
0.5mV occurs at random when nerve is at rest
39
1mEPP
1 vesicle fusion =1 quantum=10000ACh
40
1EPP
100mEPP therefore 100 vesicles
41
safety factor of neurones
margin of 200-300 vesicle releases for normal a.p at NMJ
42
what does acetylcholine break down into?
choline + acetate reforms via acetyl coA
43
acetylcholinesterase location
junctional folds in the synaptic cleft
44
acetylcholinesterase function
cleaves ACh so action potentials aren't transient
45
curare
South American arrow poison causing paralysis by blocking ACh receptor also used as muscle relaxant by anaesthetists
46
botulinum toxin
inhibits exocytosis so ACh release is blocked used in botox bacteria in tinned food
47
myasthenia gravis
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
sarcoplasmic reticulum
protein pumps transport Ca2+ ions into T-tubules
49
T-tubules
deep infoldings in sarcolemma get a.p. into parts of muscle that membrane can't reach
50
muscle fibre size
roughly 100micrometers
51
what happens during muscle contraction to muscle
shortens myosin/ actin don't change length actin slides over myosin (thick)
52
Z-line
vertical line of actin
53
M-line
vertical line of myosin
54
H band length change during contraction?
distance between actin filaments shortens
55
A band length change during contraction?
length of myosin horizontal filaments no change
56
I band length change during contraction?
distance between myosin filaments shortens
57
myosin
thick filament fibrous protein with globular head held together by M-line
58
actin
thin filaments globular protein (G-actin) linked to form chain 2 F-actin strands twist to form double helix
59
tropomyosin
fibrous protein twisted around actin
60
troponin
attached to actin at regular intervals
61
3 sub-units of actin filament
T/I > tropomyosin and actin binding C> Ca2+ binds to C, uncovering binding site
62
G-actin number of binding sites
1
63
sarcolemma
tubular structure surrounding myofibrils enlarges into terminal cisternae stores much Ca2+
64
what happens when there's an a.p in t-tubules?
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
excitogen contraction coupling
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
number of myosin heads in one muscle fibre
500
67
how many cycles per second in one muscle fibre
5
68
muscle relaxation
SR removes Ca2+ via Ca-ATPase pump ATP binds to myosin
69
3 types of neurone
motor (efferent) interneurone sensory (afferent)
70
where are interneurones located
CNS
71
types of sensory neurone
pseudo-unipolar > somatic senses bipolar> smell and vision
72
neurone characteristics
don't divide (foetal neurones lose mitosis ability) longevity high metabolic rate
73
2 types of electrical signal in neurones
action potential graded potential
74
action potential characteristics
large, uniform depolarisations travelling rapidly for long distances w/o losing strength all or none
75
graded potentials
variable strength signals that travel over short distances, losing strength can generate a.p's
76
where do graded potentials occur?
in dendrites, cell bodies or axon terminals NOT AXONS
77
depolarizing graded potential
excitatory post-synaptic potential EPSP
78
hyperpolarizing graded potential
inhibitory post-synaptic potential IPSP
79
threshold voltage
-55mV
80
subthreshold vs suprathreshold
below / reachind threshold
81
pros of frequency encoded signals
digital and therefore less prone to 'noise' greater fidelity
82
divergence
presynaptic neurone branching to affect large number of postsynaptic neurones
83
convergence
large number of presynaptic neurones converge to affect smaller number of postsynaptic neurones
84
spatial summation
EPSP's originating simultaneously at different locations on the neurone to form suprathreshold signal and therefore an a.p.
85
postsynaptic inhibition
EPSP's diminished by summation with an IPSP, meaning summed potential is subthreshold and therefore no a.p.
86
temporal summation
summation occurring from graded potentials overlapping in time
87
postsynaptic integration/ modulation
evaluation of strength / duration of signals to determine action potential firing
88
presynaptic modulation characteristics
more precise excitatory/ inhibitory
89
presynaptic similarities
action potential Ca2+ channel opening and Ca2+ increases in concentration to cause exocytosis neurotransmitter diffuses across cleft
90
postsynaptic differences
neurotransmitter identity receptor identity and mechanisms
91
neurotransmitter examples
ACh amines amino acids polypeptides purines gases
92
2 receptor mechanisms
ligand-gated ion channels (inotropic) G-protein coupled receptors (metabotropic)
93
inotropic channel characteristics example
fast synaptic potential e.g. nicotinic
94
metabotropic channel characteristics example
activates 2nd messenger systems slow synaptic potential e.g. muscarinic
95
advantage of inotropic/ metabotropic receptors
adds diversity to the system
96
synaptic plasticity
variation of electrical activity, causing rearrangmenets of circuit connections
97
long-term potentiation
process by which repetitive stimulation at a synapse increases the efficacy of transmission at that synapse
98
where was LTP first observed?
in the hippocampus
99
how is LTP prevented?
by Ca2+ removal from extracellular medium
100
main excitatory transmitter in CNS
glutamate
101
LTP process
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
AMPA
Na+ channel triggering EPSP
103
NMDA
blocked by Mg2+ therefore no effect