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Neuro > Action Potentials > Flashcards

Action Potentials Flashcards

1
Q

What are the 3 kinds of communication between neurons?

A

Modulatory, inhibitory and stimulatory

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2
Q

Where can neurones synapse?

A

With one or more neurones on their axons, cell bodies, dendrites

Or with other cell types (e.g. muscle)

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3
Q

Name the 2 different types of synaptic pathways

A

Convergent: More than one neurone synapse (can be a mix of excitatory and inhibitory) with a neuron

Divergent: One neurone synapses with multiple other neurones

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4
Q

Describe the general path inputs take after reaching the post synaptic neurons

A

Inputs reach the soma –> axon hillock determines whether the action potential will go down axon –> AP travels down axon–> synapse with another cell

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5
Q

What is the resting membrane potential of neurones and how is it maintained?

A

-60-70mV

Lipid bilayers that make up membranes are essentially impermeable to ions

However at rest there is an imbalance of various ions across the plasma membrane

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6
Q

List the relative concentrations of the most important ions in the neuron and how they are kept at this concentration

A

Na+ is higher extracellularly than intracellularly: 3Na+/2K+ ATPase

K+ is lower extracellularly:3Na+/2K+ ATPase allows K+ to go into the cell and K+ channel allows it to go out

Ca2+ is higher extracellularly:Ca2+ ATPase
and 3Na+/Ca2+ antiporter

Cl- is higher extracellularly: K+/Cl- transporter (symporter)

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7
Q

What are the 3 kinds of ion transporters? Explain

A

Uniporters: Transport one species down its concentration gradient

*next two utilise one species moving down gradient to drive the other up its gradient

Symporters:2 species in same direction
Antiporters: 2 species in opposite directions

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8
Q

Explain how the uniporter works

A

It is based on random conformational change to transporter. If concentration of X is higher on one side more will bind that side. More X is released on the side of lower conc.

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9
Q

Give an example of a uniporter

A

GLUT-1

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10
Q

Explain how a symporter works

A

(Assume X goes down its gradient and thus drives Y)

  1. X binds
  2. The affinity for Y increases
  3. Y which is in low concentration binds
  4. Conformational change og transporter
  5. X is released
  6. Affinity for Y decreases
  7. Y is released in area of high conc.
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11
Q

Give an example of a symorter

A

Glutamate dopamine transporters (DAT) : neurotransmitter reuptake at the nerve terminal (takes Na into the cell down its gradient and uses this to drive glutamine against its gradient)

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12
Q

Explain how antiporters work

A

(Assume X goes down its gradient and thus drives Y)

  1. X binds
  2. The affinity for Y decreases
  3. Y is released
  4. Transporter changes conformation
  5. X is released
  6. Affinity for Y increases
  7. Y binds
  8. conformational change
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13
Q

Give an example of an antiporter

A

VMAT2 (vesicles monoamine transporter 2): small synaptic vesicle neurotransmitter uptake for dopamine

(Uses the gradient of H+ to pump dopamine into the vescicle)

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14
Q

How do ion pumps differ from transporters?

A

They use ATP hydrolysis to influence the binding of the ion at low concentrations and release into areas of high conc (aka. up their conc. gradient)

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15
Q

How does an ion pump uniporter work?

A
  1. ATP is hydrolysed causing the affinity for X to increase
  2. X binds
  3. Conformational change
  4. Affinity for X decreases
  5. X released in area of higher conc
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16
Q

Give an example of a uniporter ion pump

A

Calcium ATPase

In the plasma membrane to decrease cytosolic calcium concentration

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17
Q

How does an antiporter pump work?

A
  1. Transporter is dephosphorylated
  2. Affinity for Y decreases while that for X increases
  3. Y released in region of high conc
  4. X binds in region of low conc
  5. Phosphorylation leads to conformational change and a reversal in affinities
  6. X is released and Y binds
  7. Dephosphorylation induces conformational change
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18
Q

Give an example of an antiporter ion pump

A

3Na+/2K+ pump (pumps Na+ out and K+ into the cell)

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19
Q

What kind of transport are transporters allowing?

A

Secondary active transport

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20
Q

Why does lack of ATP affect the cell so much?

A

Transporters use gradients set up by ATPase pumps for secondary active transport so not only the pumps but also the related transporters will cease to function

21
Q

Define ion channels

A

They are pores that:
Allow free movement of ions down their gradient.

Fast acting allowing many ions to move, but not as specific with regard which ions move as transporters and pumps

22
Q

Give examples of 2 gated ion channels

A

Voltage gated i.e. VG Na+ channel open upon depolarisation of axon

Ligand gated i.e. NMDA glutamate receptor, opens when glutamate bound, allows in Na+ and Ca2+

23
Q

What do transporters, pumps and channels have in common?

A

These are proteins that span the membrane and allow molecules/ions to cross the membrane

24
Q

How are transporters and pumps similar

A

Allow the stoichiometric (ratios) movement of ions /molecules

Are slow acting

Can move molecules against their gradient

Are relatively specific

25
Q

What is the all or nothing law?

A

Depolarisation (more +ve) is required to reach a threshold level for an action potential to fire

Above -50mV

26
Q

Describe how an action potential is generated in an axon hillock

A
  1. Axon hillock contains high levels of VG Na+ channels
  2. Depolarisation opens the Na+ channels
  3. Na+ enters approaching Na+ equilibrium
  4. VG K+ channels open and lead to efflux of K+ and hyperpolarisation (more –ve)
  5. Ion balance recovers towards E K+
27
Q

Do neurons express many different VG ion channels?

A

Yes

8 different VG Na+ channels

Several different VG K+ channels

5 different VG Ca2+ channels

28
Q

Why do neurones express so many VG ion channels

A

In order to increase the ability to regulate neural activity

29
Q

Why does the action potential have directionality?

A

Because of the absolute refractory period

30
Q

Why is there an absolute refractory period?

A

After a VG Na+ channel is activated, upon repolarisation it becomes inactive and does not allow ions through during depolatisation

31
Q

Why are VG Na+ channels a good target for antiepileptics?

A

Because they control the refractory period

32
Q

Compare naked axons to myelinated ones

A

Naked axons have poor electrical properties

AP would die out except for the VG Na+ channels along the axon

Propagation is slow as AP jumps from channel to channel

33
Q

What does myelin do?

A

Insulates the axons through decreasing leaks

Na+ channels are at nodes and propagate AP from node to node instantly, much faster

They also help nerve regeneration

34
Q

In what diseases is demyelination seen?

A

MS and peripheral nerve diseases

35
Q

When do Schwann cells develop?

A

In the embryo

36
Q

Why are teens so fast at reacting to things?

A

The Schwann cells continue to increase their wrapping around the axon throughout childhood, peaking in adolescence

37
Q

Describe the structure of a Schwann cell

A

As the cell surrounds the axon, the nucleus and other organelles are pushed to the outer side of the cell (forming the neurollema)

The inner wrapping is the myelin sheath

38
Q

How do AP in unmyelinated neurones differ compared to myelinated ones?

A

Unmyelinated is slower because APs continue down the axon as the Na+ entering the axon diffuses to the neighboring areas and causes depolarisation (leading to opening of Na+ channels and then repeat)

In myelinated: Diffusion of Na+ occurs through the area that is myelinated until it reaches a node of Ranvier and then the Na channels open there once –60mV threshold is reached (thus AP move from node to node)

39
Q

Why are channels and transporters in neurones interesting to us?

A
  • mutations can cause disease
  • toxins (e.g. snake and fish toxins) can be fatal
  • can be a target for therapy
40
Q

What part of the brain is mainly affected by channelopathies?

A

Cerebellum

41
Q

Give 3 examples of chanellopathies and their causes

A

Ataxias:

  • Cerebrospinal ataxia 6 (SCA 6) VG Ca2+ channel (CACNA1)
  • SCA13 - VG K+ KCNC3

Epilepsy:
-VG Na+ channel

42
Q

What is tetrodtoxin and how does it work?

A

Produced by puffer fish and frogs

Inhibits VG Na+ channels and can be fatal

43
Q

What can be target proteins for neuropharmacological drugs?

A

Proteins involved in :

  • Action potential
  • NT regulation
  • Neurotransmission
44
Q

What are the strategies to inhibit abnormal neuronal discharge in epilepsy?

A
  1. Inhibit voltage gated sodium channels

2. Increase GABA neurotransmission (GABA is inhibitory NT)

45
Q

What kind of neurotransmitter is GABA?

A

Inhibitory

46
Q

Why do we have to be careful with Na+ channel blocking?

A

It can be fatal if all the channels are blocked

47
Q

What is the solution to the problem of Na+ channel blocking epilepsy drugs (and how they might kill you if too potent)?

A

Use a drug which blocks the inactivated phase of the VG Na+ channel.

Inactivation of the channel is key to refractory period of neurons, and to understanding the mechanism of VGSC blockers in epilepsy

Very active neuron = many inactivated channels, so binding the drug to inactivated version can inhibit only to too reactive ones

48
Q

Name 3 antiepileptics which inhibit VGSC

A

Carbamezapine

Phenytoin

Lamotrigine

Neuro (23 decks)

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