Neuronal signalling 2 Flashcards

1
Q

membrane potential

A

the potential of the membrane of any cell

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2
Q

resting potential

A

membrane potential of a neurone not being stimulated

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3
Q

equilibrium potential

A

potential of the membrane for a single ion that stops further movement of that ion across the membrane

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4
Q

reversal potential

A

potential at which no further charge movement occurs across the membrane

for a single ion:
reversal potential = equilibrium potential

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5
Q

summation

  • define
  • what can this lead to?
A

the integration of many different EPSPs + IPSPs

when the integration is sufficiently excitatory to raise the membrane potential to threshold

  • > Na+ channels open
  • > action potential fired
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6
Q

2 mechanisms of summation

A

temporal

spatial

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7
Q

temporal summation

  • define
  • 2 effects
A

multiple stimulation at 1 synapse in a short period of time

a) graded potential doesn’t reach threshold so rapidly fades
- > cell returns to resting state

b) synapse releases neurotransmitters frequently in a short period of time
-> larger graded potential
= action potential

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8
Q

spatial summation

  • define
  • effects
A

simultaneous stimulation from 2+ nearby synapses (excitatory or inhibitory)

can have reinforcing or opposing effects

equal excitatory + inhibitory graded potentials
= cancel each other out

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9
Q

sequential opening of voltage-sensitive channels

-> leads to action potential

A

depolarisation above the threshold
-> massive opening of Na+ channels -> influx
= all or nothing spike

open K+ channels
= brief hyperpolarisation below resting potential

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10
Q

4 phases of an action potential

A
  1. Na+ channels open
    -> influx
    = depolarisation
  2. K+ channels open
    -> outflow
    = repolarisation
  3. Na+ channels inactive
    -> refractory period
    = hyper polarised
  4. Na+ channels active, but closed
    = returns to resting
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11
Q

2 types of refractory periods

A

absolute RP
= no further action potentials can be generated

relative RP
= more difficult, but some action potentials can be generated

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12
Q

restoration of the Na+ gradient

A

Na/K antiporter
exchanges 2 K+ from outside the cell
with 3 Na+ from inside the cell
using ATP

= Na+ pumped out of neurone

  • > net movement of +ve charge
  • > repolarisation
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13
Q

unequal distribution of Na+ and K+

A

membrane is more permeable to K+ than Na+
-> K+ diffuses in

Na/K pump moves Na+ out, K+ in

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14
Q

what does the Na/K anti porter maintain?

A

resting potential

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15
Q

returning to resting potential after an action potential

A

K+ channels close
repolarisation resets Na+ channels

ions diffuse away from area

Na/K antiporter maintains polarisation

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16
Q

what makes action potentials unidirectional?

A

Na+ channels go through brief inactive phases before closing

action potential cannot be fired again as the channels can’t be re-used

17
Q

2 factors that ensure propagation

A

passive properties of an axon
(electronic spread)

Na+ channel excitability

18
Q

action potential magnitude

A

all or nothing
- doesn’t vary in strength

passes undiminished as a wave along axon

19
Q

action potential

- self-propagating

A

ion movement causes depolarisation

  • > voltage-gated ion channels open
  • > more Na+ ions move in
20
Q

action potential sequence

A
  1. voltage-gated Na+ channels open
  2. Na+ influx
  3. at ~+40mV, Na+ channels close and K+ channels open
  4. outflow of K+ down electrochemical gradient
  5. K+ channels close
  6. K+ accumulates outside cell = depolarisation
  7. Na+/K+ antiporter repolarises
21
Q

propagation movement

A

sodium ions passively diffuse along the axon
-> depolarises membrane
= opening on sodium channels

22
Q

conduction velocity

A

large diameter axons
-> increases conduction velocity

myelinated neurones

  • > passive spread of ions will activate channels only at Nodes of Ranvier
  • > increases velocity
23
Q

why myelinate a neurone?

A

increases conduction velocity

size requirement is diminished

electrical insulation

reduced cell-energy requirement

24
Q

effect of myelin on neuronal size

A

an unmyelinated neurone would have to be 83x larger than a myelinated neurone to conduct the same speed

25
saltatory conduction
action potential jumps from 1 node to the next | -> travels faster than in an uncovered axon
26
neurotransmitters crossing the synapse
calcium entry causes release of neurotransmitters into the synaptic cleft -> NTs bind to receptors on the post-synaptic membrane
27
role of calcium
calcium enters through VSCC -> binds to calmodulin protein kinase - > calmodulin phosphorylates synapsin I - > synpasin I in phosphorylated form cannot bind to NT vesicles - > vesicles can now be released in to synapse
28
how do action potentials cause neurotransmitter release?
neurotransmitters stored in synaptic vesicles AP opens voltage-gated Ca2+ channels -> Ca2+ ions cause vesicles to release contents at synapse via exocytosis
29
3 types of calcium channels what are they blocked by? where are they found?
L-type > 1,4-dihydropyridine > skeletal muscle + cortex N-type > w-conotoxin > CNS/PNS P-type > w-agatoxin > cerebellum
30
types of neurotransmitters
acetylcholine amines (noradrenaline, dopamine, serotonin) amino acids (GABA, glutamate) peptides (endorphins, substance P)
31
synaptic transmission
1. action potential arrives at presynaptic membrane 2. depolarisation causes ca2+ influx 3. Ca2+ promotes exocytosis of neurotransmitter 4. nt binds to ion channels e.g. Na+ 5. EPSP spreads to spike initiation zone 6. if depolarisation reaches threshold - > spikes initiated in post-synaptic neurone
32
what is EPSP?
excitatory postsynaptic potential
33
neurotransmitter receptors - what does nt binding cause? - example of why some nts need to be degraded or cleared from the synapse? - how is ACh removed?
-> change in membrane potential due to Ca2+ entry glutamate can be toxic if not cleared degraded by an enzyme = ACh esterase
34
2 neurotransmitter receptor types
ionotropic = ligand-gated ion channels metabotropic = linked to ion channels through G protein (=GPCR)
35
ionotropic receptors examples
nicotinic acetyl-choline receptors glycine GABAa
36
metabotropic receptor examples
muscarinic acetyl-choline receptors glutamate GABAb