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NEURO > Action potentials > Flashcards

Action potentials Flashcards

1
Q

resting membrain potentions

A

= inside of cell negatively charged compared to outside

this varies from -40 to -90 mV. Typical is -70mV

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2
Q

How do Na+ and K+ ATPase pumos maintain a conc grad at resting potential

A

by pumping 3 NA+ out for every 2 K+ in
against both ions conc grads via active transport

== Na+ concentrated outside axon membrane and K+ ions concentrated inside

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3
Q

Why can’t Na+ enter cell but K+ can at resting potential`

A

`v. few Na+ voltage gated channeled are open

K+ voltage channel also closed but K+ channels (leak K+ channels) are open – = Increasing membranes permeabilty to K+ ions

= K+ diffuse out of axon down their conc gradient making inside more negative than outside

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4
Q

1) What happened when neurotransmitter binds to specific ligand-gated ion channels on post synaptic membrane

A

Na+ allowed to enter neurones

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5
Q

2) when Na+ enters neurone what happens

A

inflow of Na+ results in the inside of the neurone to become slightly more positive – INITIAL DEPOLARISATION

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6
Q

3) What does intimal depolarisation cause

A

Stimulates the opening of some VOLTAGE-GATED Na+ channels, resulting in further entry of Na+ ions into the neurone and thus further depolarisation

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7
Q

4) what happens when membrane reaches critical threshold potential (-55mV)

A

Depolarisation becomes a +ve feedback loop – Na+ entry causes depolarisation which opens more voltage gated Na+ channels, which results in more depolarisation ….

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8
Q

5) what happened when membrane potential reaches +30mV (reverse polarisation)

A

Voltage gated Na+ channels are inactivated and Na+ influx stops

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9
Q

6) What happened when the influx of na+ stops

A

‘sluggish’ voltage gated K+ channels open in delayed response to depolarisation = K+ diffuses out of neurone, down its conc grad, = neurone rapidly depolarise back to resting potential

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10
Q

7) what happened after return of neurone to -ve potential

A

Voltage gated K+ channels close but they close slowly

therefore membranes permeability to K+ remains above resting levels = continued outflow of K+ = inside of neurone more negative than -70mV = HYPER POLARISATION

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11
Q

8) What happens after hyper polarisation

A

once voltage gates K+ channels close resting potential = restored

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12
Q

Absolute refractory period

A

period when voltage gated Na+ channels either already open or have proceeded to inactivated state after first action potential, and no second action potential can be produced (regardless of stimulus strength)

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13
Q

Relative refractory period

A

After absolute refractory period where second action potential can only be produced if the stimulus strength is considerable greater than usual.

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14
Q

Why is there a refractory period

A

limits the no. of action potentials that an excitable membrane can produce in a given period of time.

Allow action potentials to be separated so that individual electrical signals are able to pass down the axon

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15
Q

1) how does a current flow

A

due to difference in potential between the depolarised membrane and adjacent segments at resting potential

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16
Q

2) how does a current flow

A

depolarises adjacent membrane where it causes voltage gated Na+ channels located there to open - resulting in action potential

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17
Q

3) how does a current flow once action potential has been caused

A

current entering during action potential is sufficient to easily depolarise adjacent membrane to threshold potential

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18
Q

Propagation along a membrane depends on

A

fibre diameter and myelination

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19
Q

Why does larger fibre diameter = faster action potential

A

bc larger fibre offers less internal resistance to local current meaning adjacent regions of the membrane are able to reach threshold faster

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20
Q

Why dies myelination increase propagation speed

A

bc there is less ‘leakage’ of charge across the myelin meaning a local current can spread farther along an axon

also conc of Na+ channels in the myelinated region of he axon is low = action potentials can only occur at the nodes of ranvier where the myelin coating is interupted and the conc of voltage gated Na+ channels is high.

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21
Q

Saltatory conduction

A

action potentials appear to jump from one node to the next as they propagate along a myelinated fibre

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22
Q

In propagation of neurones with the same axon diameter how much does it vary between unmyelinated and myelinated

A

0.5m/s in small diameter unmyelinated

100m/s in large diameter myelinated firbres

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23
Q

What is multiple sclerosis

A

Degeneration of myelin and development of scar tissue which in turn disrupts and eventually blocks neurotransmission along myelinated axons

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24
Q

`Symptoms of MS

A
  • uncontrolled eye movements - seeing double
  • slurred speech
  • Partial/ complete paralysis
  • tremor
  • loss of coordination
  • weakness
  • sensory numbness, prickling, pain
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25
Q

What is a synapse

A

specialised junction between two neurones at which the electrical activity in a presynaptic neurone influences the electrical activity of a post synaptic neurone

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26
Q

what is an EXCITATORY SYNAPSE

A

where the membrane potential of a postsynaptic is brought closer to threshold (depolarised)

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27
Q

What is an INHIBITORY SYNAPSE

A

where the membrane potential of a post synaptic neurone is either driven further from threshold (hyper polarised) or stabilised at its resting potential

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28
Q

2 types of synapse

A
  • electrical

- chemical

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29
Q

what are the plasma membranes of the pre synaptic and post synaptic membranes joined in electrical synapses

A

gap junctions

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30
Q

Why are electrical synapses joined by gap junctions

A

these junction allow the local currents resulting from arriving action potentials to flow directly across the junction through the connecting channels from one neurone to another

This depolarises the membrane of the second neurone to threshold contingent the propagation of the action potential

communication between cells via electrical synapses is extremely rapid

they also allow for synchronised transmission

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31
Q

where are electrical synapses found

A

brainstem neurones eg breathing any hypothalamus eg hormone secretion

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32
Q

`How are plasma membranes of pre synaptic and post synaptic neurones joined in a chemical synapse

A

synaptic cleft

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33
Q

Where are neurotransmitters found in chemical synapses

A

The axon of the presynaptic neurone ends in a slight swelling - the axon terminal, which holds the synaptic vesicles that contain neurotransmitter molecules

34
Q

What does the synaptic cleft do in chemical synapse

A

separates pre and post synaptic neurones and prevents direct propagation of the current.

35
Q

`How are signals transmitted across the synaptic cleft in a chemical synapse?

A

By neurotransmitter which is released by the pre synaptic axon terminal

36
Q

What is a co transmitter

A

wen more than one neurotransmitter is simultaneously released from an axon. the additional one is the co transmitter

37
Q

What cells are synapses covered by and why is this important

A

covered by ASTROCYTES- essential for the repute of excess neurotransmitter

38
Q

1) What happens when an action potential reaches the presynaptic terminal

A

calcium ion channels open and Ca2+ ions released into knob

39
Q

2) what does influx of Ca2+ cause in presynaptic membrane

A

cause vesicles containing neurotransmitter to move to release sites and fuse with the presynaptic cell membrane and discharge their contents

40
Q

3) what happened when neurotransmitter is discharged into synaptic cleft

A

neurotransmitter diffuses across the synaptic cleft and attached to receptors sites on the post synaptic membrane

note: the higher the conc of neurotransmitter released the more likely there will be binding to receptors and thus action potential propagation

41
Q

5 process of synaptic transmission

important to know since almost all drugs that act on the brain interact with one or more of these processes

A

1 MANUFACTURE - intracellular biochemical processes

2 STORAGE - vesicles

3 RELEASE - action potential

4 INTERACT W POST SYNAPTIC RECEPTORS (RECEPTOR ACTIVATION) - diffusion across synapse

5 INACTIVATION - breakdown/ reuptake

42
Q

Where is neurotransmitter used

A

Brain and neuromuscular junction

43
Q

2 main types of ACh receptors

A
  • muscarinic

- nicotinic

44
Q

What happens once ACh has bound to the post- synaptic receptor

A

The enzyme acetylcholinearase breaks it down into acetyl and choline

chilling then reabsorbed by the presynaptic neurone to be used to make more acetylcholine

45
Q

once neurotransmitters have been released only a fraction of them bind on the post synaptic neurone these can take the form of TRANSMITTER GATED ION CHANNELS
these are sensitive to..

A

SPECIFIC neurotransmitters

46
Q

When neurotransmitters bind to the channels on the post synaptic membrane it results in depolarisation or hyper polarisation depending on the channel type:

A

1 DEPOLARISATION - will occur in excitatory channels (excitatory post-synaptic potential) - EPSP, many Na+leave and few K+ Enter

2 HYPERPOLARISATION - Will occur in inhibitory channels (inhibitory post-synaptic potential) - IPSP, many K+ leave OR many Cl- enter

47
Q

once a neurotransmitter has bound it will result in a an action potential IF WHAT

A

it is an excitatory channel

48
Q

Temoral summation

A

input signals arrive from the same presynaptic cell at different times. The potentials summate since there are a greater number of open ion channels and thus a greater flow of positive ions into the cell

49
Q

Spatial summation

A

Where two inputs occur at different locations in the post synaptic neurone

50
Q

Why are spatial and temporal summation important

A

Interaction of multiple EPSPs through spatial and temporal summation can increase the inward flow of +ve ions and bring the postsynaptic membrane to threshold so that action potentials are initiated

51
Q

When are unbound neurotransmitters removed from the synaptic cleft?

A

1 They are actively transported back into the presynaptic axon terminal (through process called reuptake) or in some cases by nearby glial cells

2 They diffuse away from receptor site

3 Are enzymatically transformed into inactive substances, some are transported back into the presynaptic neurone for reuse

52
Q

give examples of fast neurotransmitters ; short lasting effects, tend to be involved in rapid communication

A

Acetylcholine (ACh)
Glutamate (GLU) - excitatory
GABA - inhibitory

53
Q

What do neuromodulators do

A

cause change in synaptic membrane that last for longer time e.g. minutes, hours, or even days inc alterations in enzyme activity or influences DNA transcription in protein synthesis
associated with slower events e.g. learning, development, motivational states etc

54
Q

Example of neuromodulators

A
  • Dopamine (DA)
  • Noradrenalin (NA) or norepenephrin
  • Serotonin
55
Q

Most common anaesthetics

A

Procaine and Lignocaine

56
Q

How do anaesthetics work

A

interrupting axonal transmission

They do this by blocking sodium channels, thereby preventing the neurones from depolarising meaning threshold isn’t met and thus no action potential is developed to be propagated

= pain relief bc no pain transmitted

Local anaesthetics can diffuse through mucus membranes easily thus sometimes act on muscles too

57
Q

What are choleric neurones

A

neurones that release ACh

58
Q

What is the major neurotransmitter if the PNS at the neuromuscular junction and where else is it also used

A

Acetylcholine and also used in the brain and spinal cord

59
Q

What is ACh synthesised from and where

A

choline (common nutrient found in food) & Acetyl CoEnzyme A in the cytoplasm of synaptic terminals and stores in synaptic vesicles

60
Q

What happens after ACh is released into synaptic cleft

A

After it is released and activated the receptors of the post synaptic membrane the conc of ACh at the post synaptic membrane decreases thereby stopping receptor activtion , due to the action of the enzyme acetylcholinestrase

61
Q

Where is acetylcholinesterase located

A

on the postsynaotic and presynaptic membraned and rapidly destroys ACh, releasing choline and acetate

62
Q

What happened when acetylcholine is broken down

A

choline is transported back into the presynaptic axon terminal where it is reused in the resynthesis of ACh

63
Q

2 types of ACh receptors

A

Nicotinic

Muscarinic

64
Q

how do nicotinic receptors work

A

since these respond to nicotine as well as ACh , this receptors contains an ion channel. Found in the neuromuscular junction.
nicotinic receptors in the brain are important in cognitive functions and behaviour e.g. one cholinergic system that employs nicotinic receptors plays a major role in attention, learning and memory by reinforcing the ability to detect and respond to meaningful stimuli.
The presence of nicotinic receptors of presynaptic terminals in reward pathways of the brain explains why tobacco products are so productive. `

65
Q

How do muscarinic receptors work

A

Since they respond to mushroom poison, Muscarine, as well as ACh. These receptors couple with G-proteins, which in turn alter the activity of a number of different enzymes and ion channels.
These receptors are present in the brain and at junctions where a major division of the PNS innervates peripheral organs and glands e.g. saliva glands and the heart and lungs (bronchoconstriction)

66
Q

what do cigarettes contain and what is this

A

nicotine - which are agonists - able to interact and open receptor

67
Q

How does Sarin work

A

Inhibit the action of acetylcholinesterase thereby causing a build up of ACh in the synaptic cleft = overstimulation of post synaptic ACh receptors, initially causing uncontrolled muscle contractions but eventually leading to receptor desensitisation and paralysis

68
Q

What is noradrenalin

A

transmitter in the peripheral heart and CNS

69
Q

How is noradrenalin affected by the antidepressant Imipramine

A

Blocks the re uptake of noradrenaline.
Therapeutic effect is only seen after 3-5 weeks, since the blockage of reuptake DOES NOT cause the therapeutic effect - instead the brains response to this does

70
Q

How is noradrenalin affected by the antidepressant Monoamine Oxidase (MAO) inhibitor

A

increases the amount of noradrenaline by inhibiting the enzyme monoamine oxidase which is the enzyme used to break down noradrenaline

71
Q

How is noradrenalin affected by the stimulant amphetamine

A

increases the release and blocks re uptake

72
Q

Dopamine is an important neurotransmitter where

A

basal ganglia

73
Q

How is dopamine affected by antipsychotic drugs e.g. chlorpromazine

A

chlorpromazine is an antagonist

- blocks receptor so other neurotransmitter cannot activate receptor

74
Q

How is dopamine affected by stimulants e.g. amphetamine/ cocaine

A

Increases releases and blocks re uptake

75
Q

How is dopamine affected by Anti parkinsons drug : L-DOPA

A

increases dopamine manufacture

76
Q

Function of serotonin

A

has an excitatory effect on pathways that mediate sensations

77
Q

How is serotonin affected by antidepressant e.g. prozac

A

SELECTIVE SEROTONIN REUPTAKE INHIBITOR (SSRI)

resulting in an increase in the conc of synaptic serotonin

78
Q

How is serotonin affected by ecstasy

A

neurotoxic to serotonin neurones (destroy the terminal axons)

79
Q

What is the main EXCITATORY neurotransmitter

A

GLUTAMATE

80
Q

What is the main inhibitory neurotransmitter

A

GABA

81
Q

What happens in parkinsons disease

A

degradation/death of dopaminergic neurones

82
Q

Why is L-Dopa given to patients and how does it work

A

its a precursor for Dopamine

It is able to cross the BBB and is taken up by serotonin neurones and converted & released as dopamine, due to the fact that serotonin neurones contain the same enzyme need to convert L-DOPA to dopamine ad the dopaminergic neurones have.

NEURO (9 decks)

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