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BRS > Neuro - NTs and Pharmacology > Flashcards

Neuro - NTs and Pharmacology Flashcards

1
Q

What features of the nervous system underpin synaptic transmission?

A

Diversity and plasticity of nervous system

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2
Q

What do spines on dendrites do?

A

Increase surface area

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3
Q

What are dendrites concerned with?

A

Information reception

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4
Q

What does the soma do?

A

Integration of multiple signals form different NTs

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5
Q

What is the axon/synaptic terminal involved in?

A

Rapid transmission of the AP and NT release

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6
Q

How fast is neurotransmission?

A

2ms

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7
Q

How wide is a normal synaptic cleft?

A

20-100nm

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8
Q

What are the 3 main stages of synaptic transmission?

A

1 Biosynthesis
2 Receptor action
3 Inactivation

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9
Q

What are the three main molecules that make up NTs?

A

Amino acids
Amines
Neuropeptides

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10
Q

What is an example of NTs that are amino acids

A

Glutamate
GABA
Glycine

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11
Q

What is an example of NTs that are amines

A

DA

NA

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12
Q

What is an example of NTs that are neuropeptides

A

opioid peptides e.g. endorphins

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13
Q

What kinds of effects do NTs evoke?

A

Rapid or slower effects

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14
Q

How many NT influences are received simultaneously by a neurone?

A

Multiple, which are then integrated into 1 diverse signal in the 2nd cell.

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15
Q

How are calcium channels opening in the presynaptic terminal?

A

From both a sodium influx and potassium efflux as a result of depolarisation from AP

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16
Q

What does the intracellular volume of calcium increase to?

A

from 1µM —-> 200µM

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17
Q

What does NT release depend upon?

A

Calcium dependent and rapid transduction

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18
Q

Is neurotransmission active or passive?

A

Active - requires ATP

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19
Q

How are synaptic vesicles filled with NTs?

A

Protein pumps pump from 4,000 to 10,000 NTs into a vesicle

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20
Q

What happens after the influx of calcium?

A

Vesicles containing NTs dock and are primed at the edge of the knob, but only release when they fuse with the membrane with the help of vesicular proteins.

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21
Q

What is the role of vesicular proteins?

A

Help the fusing of the vesicles with the membrane of the presynaptic terminal

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22
Q

What is an example of a vesicular protein?

A

SNARE proteins: synapsin

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23
Q

What is alpha latrotoxin?

A

Neurotoxin - stimulates NT release until the presynaptic neurone is depleted of NTs

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24
Q

Where is alpha latrotoxin found?

A

Black Widow Spider Venom - causes ACh release and eventual paralysis.

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25
Q

What are zinc dependent endopeptidases?

A

inhibit NT release

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26
Q

What is an example of a zinc dependent endopeptidase?

A

Tetanum toxin from C.Tetani - causes spasms and paralysis as it inhibits GABA and Glycine release which are inhibitory

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27
Q

Where is the botulinum toxin come from?

A

C.Botulinum

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28
Q

What is the effect of botulinum toxin?

A

Causes flaccid paralysis - first part of molecule binds to nerve terminal and the 2nd part penetrates the cholinergic terminal and cleaves the peptide bonds of vesicular proteins to inhibit NT release

29
Q

How does botulism cause death?

A

Respiratory arrest

30
Q

What is c.botulinum used for commercially?

31
Q

What are the 2 main classes of receptor?

A

Ion channel linked

G-protein coupled

32
Q

How fast do ion channel linked receptors act?

A

Fast (milsecs)

33
Q

How fast do g-protein coupled receptors act?

A

Slow (seconds to minutes)

34
Q

What do ion-channel linked receptors mediate?

A

All fast, excitatory and inhibitory transmissions

35
Q

What do G-protein coupled receptors mediate?

A

All slow reactions

36
Q

What may G-protein coupled receptors be in the form of?

A

Enzymes or channels

37
Q

What is an example of an ion channel inked receptor?

A

Glutamate receptor - allows for the opening of sodium channels to allow for depolarisation and propagation of the AP.

38
Q

How do G-protein coupled receptors work?

A

First couples to the G protein which then links to the effector to induce a response in the effector

39
Q

What is an example of a G-protein coupled receptor?

A

ACh muscarinic receptors

40
Q

What is the structure of ion channel inked receptors?

A

5 subunits with distinct properties on each one.

41
Q

What is the glutamate receptor?

A

Excitatory ion channel inked receptor linked to depolarisation

42
Q

What is the GABA-A receptor?

A

Inhibitory ion channel inked receptor linked to hyperpolarisation

43
Q

What is the EPSP?

A

Excitatory post synaptic potential after the binding of glutamate

44
Q

What is the IPSP?

A

Inhibitory post synaptic potential after the binding of GABA

45
Q

What must there be between the EPSP and is the IPSP?

46
Q

What is the AMPA receptor?

A

Type of glutamate receptor

47
Q

What does the AMPA receptor mediate?

A

Majority of fast excitatory synapses

48
Q

How is the AMPA receptor closely regulated?

A

Rapid onset, offset and desensitisation

49
Q

What is the NMDA receptor?

A

Glutamate receptor that’s permeable to Calcium as well as Sodium

50
Q

What do NMDA receptors do?

A

Provide the slow component of excitatory transmission

51
Q

How do NMDA receptors serve as coincidence detectors?

A

Underlie learning and memory mechanisms (e.g. hippocampus has a high concentration of NMDA receptors)

52
Q

How is glutamate produced?

A

By glucose via the TCA cycle and transamination in the presynaptic terminal.

53
Q

How does glutamate act as a neurotransmitter?

A

Reversibly binds to post synaptic receptors to eventually induce a post synaptic response

54
Q

What happens after glutamate binds to receptors?

A

It is inactivated by reputake into the presynaptic cells and glutamate transports found in glial cells + presynaptic terminal

55
Q

What are EAATs?

A

Excitatory amino acid transporters

56
Q

What is the glutamate-glutamine cycle?

A

Glutamate is converted to glutamine via glutamine synthetase. A high concentration of glutamine is then released by glial cells and pumped back into the presynaptic terminal

57
Q

What is commonly associated with excess glutamate found within the synapse?

58
Q

How do things return to normal after a seizure?

A

Glutamate levels slowly fall as it is converted to glutamine

59
Q

How is epilepsy characterised?

A

Recurrent seizures due to abnormal neuronal excitability

60
Q

How many epilepsy patients are refractory to treatment?

61
Q

What do we believe to be the underlying problem with many cases of epilepsy?

A

GABA transmission (inhibitory) may not be functioning correctly allowing excess glutamate activity to occur

62
Q

How is GABA synthesised?

A

Decarboxylation of glutamate via glutamic acid decarboxylase in the presynaptic terminal

63
Q

How does GABA cause hyperpolarisation?

A

Binds to GABA-ARs to induce chloride influx into cells so that the cell is less sensitive to the Action potential, as its MP is brought down lots.

64
Q

What happens to GABA after binding to GABA-A receptors?

A

Reuptake of GABA via GABA transporters (GATs) in presynaptic terminal or modification by GABATS

65
Q

What are GABATs?

A

GABA transaminase which modified GABA to succinic semialdehyde which is the converted to succinate for the TCA cycle

66
Q

Where does conversion of GABA to succinic semialdehyde take place?

A

Typically glial cells, but excess GABA in cells means that the presynaptic terminal will take up some GABA too with GABATS

67
Q

What is the structure of a GABA receptor?

A

Pentameric

68
Q

How are drugs tailored towards GABA receptor structure

A

Different drugs can bind got different sub units of GABA A receptor - many of them facilitate GABA transmission to improve its function.

69
Q

What’s an example of anti-epileptic drugs?

A

Barbiturates

BRS (16 decks)

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