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Medicine Lectures- Neuro > Cell to Cell Communication in the Nervous System > Flashcards

Cell to Cell Communication in the Nervous System Flashcards

1
Q

What is the axon hillock?

A

The root of the axon

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2
Q

What is found at the axon hillock?

A

Depolarising electrotonic potentials that spread down from the dendrites

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3
Q

What direction does the action potential go in?

A

From the cell body to the axon terminals

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4
Q

What can increase the speed of action potential propagation?

A
  • larger diameter

- low membrane permeability

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5
Q

How does a larger diameter increase the speed of action potential propagation?

A
  • less resistance to current flow
  • more likely to spread faster
  • the further it goes, the faster the AP will propagate
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6
Q

How does a low permeability increase the speed of action potential propagation?

A
  • has myelin sheath to provide insulation
  • no leak channels or voltage-gated channels
  • means no leakage of K+ to cause repolarisation
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7
Q

What is saltatory conduction?

A

Jumping of APs from node to node (nodes of Ranvier)

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8
Q

What happens if the myelin sheath is damaged/lost and what is the medical term for this?

A
  • transmission is delayed/blocked
  • axon is more leaky
  • medical term is multiple sclerosis
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9
Q

What happens during multiple sclerosis?

A

Plaques develop in the CNS white matter which produces sensory/motor/cognitive/behavioural defects

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10
Q

What type of synapse is found in the heart and how does this work?

A

Electrical synapses

  • axon terminal of one cell is very close to membrane of post-synaptic cell
  • channel proteins can punch through both membranes and couple them together
  • causes direct depolarisation of the post-synaptic cell
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11
Q

What are the 3 ways in which neurotransmitters are synthesised?

A

Synthesis in cell body
Local synthesis
Created within axon terminals

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12
Q

What is an example of a neurotransmitter that is synthesised in the cell body?

A

Neuropeptides

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13
Q

How do neurotransmitters travel to the axon terminal after being synthesised in the cell body?

A

Carried down to terminals via microtubules that form the intracellular skeleton of axon

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14
Q

Which neurotransmitters are synthesised locally?

A

Catechocamines like dopamine and norepinephrine

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15
Q

How are neurotransmitters synthesised within axon terminals?

A

The axon terminal contains enzymes needed for its synthesis

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16
Q

What is the intermediate produced when dopamine and norepinephrine react together?

A

L-DOPA

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17
Q

What is the effect of giving L-DOPA

A

It increases the rate of production which boosts the effectiveness of these synapses

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18
Q

How is the neurotransmitter released from the pre-synaptic bouton?

A
  1. AP arrives at pre-synaptic bouton which causes Ca2+ channels to open
  2. Calcium used as intracellular signalling, more calcium outside than inside so due to the conc gradient, calcium moves in
  3. Proteins hold vesicles with neurotransmitters in them and pull them down to the membrane
  4. When Ca2+ enters it binds to the proteins and causes proteins to force vesicles to fuse with the membrane
  5. Vesicle turns inside out and neurotransmitter is released by exocytosis as the membrane bit of the vesicles returns back to the membrane
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19
Q

How do cells maintain a 0mM of calcium ions in their ICF?

A

Done by pumping calcium ions out and by sequestering (isolating/hiding) calcium ions inside. This forms a concentration gradient

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20
Q

What is the effect of botulinum toxin?

A

Blocks neuromuscular transmission by interfering with the Ca2+-dependent release mechanism
This prevents the release of the neurotransmitter
So the signal is not passed on

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21
Q

What are the 2 receptors that are found on post-synaptic membranes?

A

Metabotropic/G-protein coupled (slow)

Ionotropic/Ligand-gated (fast)

22
Q

What are the features of ligand-gated receptors?

A
  • fast
  • time-dependent transmission
  • activated by neurotransmitters
23
Q

What does the excitatory synapse do in a ligand-gated receptor?

A

It allows Na+ through

Produces an EPSP

24
Q

What are examples of excitatory synapses and what neurotransmitter do they use?

A

NMJ- uses acetylcholine

CNS- uses glutamate

25
Q

What does the inhibitory synapse do in a ligand-gated receptor?

A

It allows Cl- through

Produces an IPSP

26
Q

What are examples of inhibitory synapses and what neurotransmitter do they use?

A

Cerebral cortex- uses y-aminobutyric acid (GABA)

Spinal cord and retina- uses glycine

27
Q

What does a lack of GABA result in?

A

Epilepsy

28
Q

What are the features of metabotropic receptors?

A
  • slow

- non-time-dependent effects

29
Q

Where are metabotropic receptor pathways found?

A

In the brain

30
Q

Which neurotransmitters act at metabotropic receptors?

A

Dopamine, Ach, serotonin and norepinephrine

31
Q

How do G-protein coupled receptors work?

A
  1. Binding of neurotransmitter
  2. Activates G-protein
  3. G-proteins can:
    - open channels
    - make second messengers
    - change protein synthesis
32
Q

What are the effects of drugs on receptors?

A

Can either bind on same site as neurotransmitter and have excitatory/inhibitory effects
Or they can bind to other sites on receptors and modify their response (increase/decrease the response to natural neurotransmitters

33
Q

Which type of receptor are drugs mainly targeted at and why? Give examples

A

More targeted at metabotropic receptors as they produce relatively subtle effects and are therefore safer targets
e.g. beta blockers and anti-depressants

34
Q

Why is the removal of neurotransmitters from the synaptic cleft necessary?

A

As we don’t want it to have a lingering effect

35
Q

What are the 3 ways that a neurotransmitter can be removed from the synaptic cleft?

A

Enzyme degradation
Sucked back into pre-synaptic bouton
Taken into nearby glial cells

36
Q

Which enzyme is used to remove Ach from the synaptic cleft?

A

Acetylcholinesterase (AchE)

37
Q

What is the effect of AchE inhibitors and which patients receive these?

A

They increase cholinergic transmission, prevent AchE from removing Ach from the synaptic cleft= increased effect of Ach
Used in patients with Alzheimer’s

38
Q

What happens after some neurotransmitters are sucked back up into the pre-synaptic bouton?

A

They’re packaged back into vesicles

39
Q

What are examples of neurotransmitters that are taken back into the pre-synaptic bouton?

A

Dopamine, serotonin, norepinephrine

40
Q

What is an example of a dopamine inhibitor and what is its effect?

A

Cocaine= longer feeling of pleasure

41
Q

What is the effect of anti-depressants?

A

They are also known as selective serotonin reuptake inhibitors (SSRIs) and they make you feel more positive

42
Q

What are examples of neurotransmitters that are taken into nearby glial cells?

A

GABA and glutamate

43
Q

What type of receptors do GABA and glutamate work at?

A

Ionotropic

44
Q

Why are GABA and glutamate removed from the synaptic cleft?

A

As the pattern of APs fired might encode information that needs to be transmitted from one cell to another as cleanly as possible

45
Q

What happens to the neurotransmitters after they’ve been taken up into the glial cells?

A

The glial cells transport it back to the terminals

46
Q

What happens during hypoxia?

A

Glutamate stays in the synaptic cleft which is toxic and therefore kills cells

47
Q

What happens to useful synapses vs not useful synapses?

A

Useful synapses are strengthened so if an excitatory synapse is activated, the post-synaptic cell is strongly depolarised
Not useful synapses are weakened so the activation of an excitatory synapse only produces a little EPSP, less neurotransmitters are produced/released and it loses receptors

48
Q

Where in the body do excitable cells fire spontaneous bursts of APs?

A

Heart and CNS

49
Q

Why do excitable cells fire spontaneous bursts of APs?

A

Due to an unstable membrane potential

50
Q

Why is it important that synapses are weak?

A

As one nerve cell receives APs from lots of different sources

Medicine Lectures- Neuro (5 decks)

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