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Neuroscience > Neuronal signalling 2 > Flashcards

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
Q

saltatory conduction

A

action potential jumps from 1 node to the next

-> travels faster than in an uncovered axon

26
Q

neurotransmitters crossing the synapse

A

calcium entry causes release of neurotransmitters into the synaptic cleft

-> NTs bind to receptors on the post-synaptic membrane

27
Q

role of calcium

A

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
Q

how do action potentials cause neurotransmitter release?

A

neurotransmitters stored in synaptic vesicles

AP opens voltage-gated Ca2+ channels
-> Ca2+ ions cause vesicles to release contents at synapse
via exocytosis

29
Q

3 types of calcium channels

what are they blocked by?

where are they found?

A

L-type
> 1,4-dihydropyridine
> skeletal muscle + cortex

N-type
> w-conotoxin
> CNS/PNS

P-type
> w-agatoxin
> cerebellum

30
Q

types of neurotransmitters

A

acetylcholine

amines
(noradrenaline, dopamine, serotonin)

amino acids
(GABA, glutamate)

peptides
(endorphins, substance P)

31
Q

synaptic transmission

A
  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
Q

what is EPSP?

A

excitatory postsynaptic potential

33
Q

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?
A

-> change in membrane potential due to Ca2+ entry

glutamate can be toxic if not cleared

degraded by an enzyme
= ACh esterase

34
Q

2 neurotransmitter receptor types

A

ionotropic
= ligand-gated ion channels

metabotropic
= linked to ion channels through G protein
(=GPCR)

35
Q

ionotropic receptors examples

A

nicotinic acetyl-choline receptors

glycine

GABAa

36
Q

metabotropic receptor examples

A

muscarinic acetyl-choline receptors

glutamate

GABAb

Neuroscience (17 decks)

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