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Neuro > Action potentials and synapses > Flashcards

Action potentials and synapses Flashcards

1
Q

what is the resting membrane potential

A

potential difference across plasma membrane

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2
Q

what is a normal resting membrane potential

A

-70mV

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3
Q

how is a resting potential established

A

Na+/K+ ATPase pumps in neurone membranes pump 3Na+ out for every 2K+ in
Membrane more permeable to K+ than Na+
Equilibrium reached at resting potential

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4
Q

why is there a difference in membrane permeability to Na+ and K+ in resting potential

A

Few VG Na+ channels open so relatively impermeable to Na+

VG K+ channels closed but leak K+ channels are open so membrane more permeable to K+

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5
Q

Describe an AP in a post-synaptic membrane

A
  • NT binds to specific ligand gated ion channels so Na+ enters and initial depolarisation occurs
  • VG Na+ channels open so further depolarisation
  • Critical threshold potential reached and depolarisation becomes positive feedback
  • reverse polarization reached so VG Na+ inactivated
  • sluggish VG K+ channels open so rapid repolarisation
  • VG K+ close slowly so hyperpolarisation
  • RP restored when VG K+ close
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6
Q

what is the approximate value of the critical threshold potential

A

-55mV

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7
Q

what is the critical threshold potential

A

when depolarisation becomes a positive feedback loop; Na+ entry causes depolarisation which means more VG Na+ channels open etc

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8
Q

what is the approximate value of the reverse polariszation

A

+30mV

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9
Q

why do VG K+ channels open

A

in response to initial depolarisation but are sluggish to open initially

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10
Q

why does hyperpolarisation occur

A

VG K+ channels close when negative potential reached but close slowly so continued outflow of K+

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11
Q

what is the absolute refractory period

A

when VG Na+ channels are already open/ inactivated after 1st AP
- no second AP can be produced regardless of strength of stimulus

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12
Q

what is the relative refractory period

A

2nd AP can be produced

  • needs much stronger stimulus
  • lasts until membrane resturns to resting potential
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13
Q

how are AP propagated

A

AP generation causes current to flow which depolarises adjacent membranes to threshold potential and causes Na+ channels to open so propagation occurs

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14
Q

what does propagation speed of AP depend on

A

fibre diameter and myelination

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15
Q

why does increasing fibre diameter increase propagation speed of AP

A

less internal resistance to local current

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16
Q

what is axonal transmission

A

transmission of information from A to B

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17
Q

What is synaptic transmission

A

integration/ processing of information

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18
Q

what is the pathophysiology of multiple sclerosis

A

degradation of myelin and development of scar tissue that eventually blocks neurotransmission along myelinated axons

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19
Q

what are the symptoms of multiple sclerosis

A 
uncontrolled eye movements
slurred speech
partial/ complete paralysis
tremor
loss of co-ordination 
weakness
sensory numbness
prickling 
pain
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20
Q

who is most commonly affected by multiple sclerosis

A

young adults

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21
Q

what is a synapse

A

specialised junction between 2 neurons where electrical activity in presynaptic neurone influences electrical activity of post-synaptic neurones

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22
Q

what is an excitatory synapse

A

membrane potential of postsynaptic membrane is brought closer to threshold

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23
Q

what is an inhibitory synapse

A

membrane potential of postsynaptic neurone hyperpolarised (brought further from threshold) or stabilised at resting potential

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24
Q

what are the 2 types of synapses

A

electrical and chemical

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25
Q

describe electrical synapses

A

gap junctions join plasma membrane of pre and post synaptic cells so local current flow directly
very rapid - synchronised transmission

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26
Q

where are electrical synapses found

A

brainstem neurons and hypothalamus

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27
Q

describe the structure of chemical synapses

A

plasma mmebranes joined by synaptic cleft that prevents direct propagation of current
presynaptic membrane has axon terminal
synapses covered in astrocytes

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28
Q

what is contained in an axon terminal

A

synaptic vesicles that store neurotransmitter molecules

29
Q

what is the name of additional neurotransmitters in a chemical synapse

A

co-transmitter

30
Q

what do astrocytes in chemical synapses do

A

reuptake of excess neurotransmitter

31
Q

Describe synaptic transmission at a chemical synapse

A
  • AP causes VG Ca+ channels in pre-synaptic terminal to open
  • vesicles move, fuse and release contents
  • NT diffuses across cleft
  • attach to receptor sites on post-synaptic membrane
32
Q

what are receptors for neurotransmitters

A

transmitter-gated ion channels

- specific

33
Q

describe excitatory channels in chemical synapse

A

excitatory post-synaptic potential (EPSP) leads to depolarisation
- many Na+ leave, few K+ enter

34
Q

describe inhibitory channels in chemical synapses

A

inhibitory post-synaptic potential (IPSP) leads to hyperpolarisation
- many K+ leave OR many Cl- enter

35
Q

what are the 3 ways unbound neurotransmitters are removed from synaptic cleft

A

Reuptake
Diffuse away
Enzymatically transported into inactive substances

36
Q

describe reuptake of NT in chemical synapse

A

active transport of NT back into presynaptic axon terminal/ nearby glial cells

37
Q

what are the 5 processes of synaptic transmission

A 
manufacture
storage
release
interact with post-synaptic receptors
inactivation
38
Q

what is temporal summation

A

input arrives from same pre-synaptic cell at different times - potentials summate because greater number of open ion channels means increased flow of positive ions into cell

39
Q

what is spatial summation

A

2 inputs occur at different locations in post-synaptic neurone

40
Q

what are the 2 classes of neurotransmitters

A

fast and neuromodulators

41
Q

describe fast neurotransmitters and give some examples

A

short lasting effects
involved in rapid communication
ACh, GLU, GABA

42
Q

what do neuromodulator neurotransmitters do

A

cause changes in synaptic membrane

43
Q

describe neuromodulators and give some examples

A

longer lasting
involved in slower events (e.g. learning, development, motivational status)
Dopamine, noradrenaline, serotonin

44
Q

what are the most common local anaesthetics

A

procaine and lignocaine

45
Q

what do local anaesthetics do

A

interrupt axonal transmission and block Na+ channels so prevent depolarisation so no AP generated

46
Q

why do local anaesthetics generate pain relief

A

pain isn’t transmitted

47
Q

name 6 neurotransmitters

A

ACh, Noradrenaline (NA), dopamine (DA), serotonin, glutamate, GABA

48
Q

Acetylcholine;

  • what neurones release it
  • what enzyme degrades it
  • what are the receptors
  • what is an example of an agonist
A

cholinergic neurons

acetylcholinesterase

nicotinic and muscarinic receptors

nicotine is an agonist

49
Q

describe what AChe does

A

breaks down ACh to acetate and choline;

choline is transported back into presynaptic axon terminal and reused to resynthesise ACh

50
Q

describe nicotinic receptors

A

respond to ACh and nicotine
contain ion-channels
in neuromuscular junctions and brain

51
Q

describe muscarinic receptors

A

respond to ACH
receptor coupled with G proteins - alter activity of different enzymes/ ion channels
in brain and junctions where major PNS divisions innervate peripheral glands/ organs

52
Q

give some specific examples of muscarinic receptors

A

M2 - heart

M3 - bronchoconstriction

53
Q

what does sarin do

A

inhibits ACHe
causes build up of ACh in synaptic cleft
overstimulation of ACh receptors leads to uncontrolled motor contractions eventually resulting in receptor desensitisation and paralysis

54
Q

where is noradrenaline found

A

peripheral heart and CNS

55
Q

what breaks down noradrenaline

A

monoamine oxidase (MAO)

56
Q

what affects noradrenaline

A

antidepressant drugs, stimulants like amphetamine

57
Q

what does amphetamine do

A

increases release of noradrenaline and blocks its reuptake

58
Q

where is dopamine found

A

basal ganglia

59
Q

what is the pathway of dopamine production

A

tyrosine converted to L-dopa which is decarboxylated to form dopamine

60
Q

where does dopamine work

A

G-protein coupled receptors

61
Q

how is dopamine removed from synaptic cleft

A

dopamine transporter

62
Q

what affects dopamine

A

antipsycotic drugs, stimulants, anti-Parkinson’s drugs

63
Q

describe anti-Parkinson’s drug

A

L-dopa increases dropamine manufacture; is dopamine precursor that is able to cross BBB - is taken up by serotonin neurons where it is converted and released as dopamine

64
Q

where does serotonin act

A

excitatory effect on pathways that mediate sensation

65
Q

what affects serotonin

A

antidepressants

ecstasy

66
Q

what is the effect of ecstasy (NT)

A

neurotoxic to serotonin neurons

67
Q

what is glutamate

A

main excitatory neurotransmitter

68
Q

what is GABA

A

main inhibitory neurotransmitter

69
Q

what does GABA stand for

A

gamma-aminobutyric acid

Neuro (11 decks)

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