Neurotransmitters Flashcards

1
Q

Define a NT (4 points)

A
  • Must be present in the presynaptic neuron
  • Must be released in response to presynaptic depolarisation
  • Release is usually Ca 2+ dependent
  • Specific receptors must be present on post-synaptic cell
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2
Q

Mechanisms of post-synaptic excitation (cell is becoming more positive)

A
  • Opening of Na channels
  • Suppression of Cl and K channels
  • EPS receptors increase in number and localisation
  • Suppression of inhibitory receptors
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3
Q

Mechanisms of post-synaptic inhibition

A
  • Increased Cl conductance
  • Increased K conductance
  • IPS receptors increase in number and localisation
  • Inhibition of cellular metabolism (< metabotropic response)
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4
Q

What effect do Cl and K channels have on the potential of the cell?

A

Cl channels let Cl INTO the cell to keep it -ve, and K channels let K OUT to keep it -ve. The more of these channels are open the harder it will be for Na to create an AP. The more of these are closed the bigger the effect of Na

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5
Q

What is the NT ACh’s post-synaptic effect?

A

Excitatory

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6
Q

What are the precursors for ACh?

A

Choline and acetyl CoA

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7
Q

What is the removal mechanism for ACh?

A

AChEase (acetylcholinesterase)

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8
Q

Glutamate has an inhibitory post-synaptic effect. (T/F?)

A

FALSE- it is excitatory

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9
Q

What is the prescursor for glutamate?

A

Glutamine

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10
Q

What is the removal mechanism for glutamate?

A

Transporters

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11
Q

What is the most important excitatory NT in the brain?

A

Glutamate

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12
Q

What are the most important inhibitory NTs in the brain?

A

Gamma-aminobutyric acid (cerebrum) and glycine (spinal cord)

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13
Q

Gamma-amino butyric acid has an excitatory post-synaptic effect. (T/F?)

A

FALSE- it is inhibitory

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14
Q

What is the precursor for GABA?

A

Glutamate

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15
Q

What is the removal mechanism for GABA?

A

Transporters

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16
Q

What is the post-synaptic effect of glycine?

A

It is inhibitory

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17
Q

Serine is the precursor for glycine (T/F?)

A

TRUE

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18
Q

What is the removal mechanism for glycine?

A

Transporters

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19
Q

What chemicals does the term “catecholamines” include?

A

Ad, NAd and dopamine

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20
Q

What post-synaptic effect do catecholamines have?

A

Excitatory

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21
Q

Tyrosine is the precursor for catecholamines (T/F?)

A

TRUE

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22
Q

What are the removal mechanisms for catecholamines?

A

Transporters, MAO, COMT

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23
Q

What are MAO and COMT?

A

Enzymes involved in metabolising catecholamine neurotransmitters.

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24
Q

What is the systematic name of serotonin? (Abbr. 5-HT)

A

5- hydroxytryptamine

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25
Q

Serotonin has an excitatory post-synaptic effect (T/F?)

A

TRUE

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26
Q

What is the precursor for serotonin?

A

Tryptophan

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27
Q

What are the removal mechanisms for serotonin?

A

Transporters, MAO

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28
Q

What does MAO stand for?

A

Monoamine oxidase

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29
Q

The post-synaptic effect of histamine is inhibitory (T/F?)

A

FALSE- it is excitatory

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30
Q

What is the pre-cursor for histamine?

A

Histidine

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31
Q

What is the removal mechanism for histamine?

A

Transporters

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32
Q

What is the post-synaptic effect of ATP?

A

Excitatory

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33
Q

What is the precursor for ATP?

A

ADP

34
Q

What is the removal mechanism for ATP?

A

Hydrolysis to AMP and adenosine

35
Q

What type of neurotransmitter includes ACh, glutamate, GABA, glycine, catecholamines, serotonin, histamine and ATP?

A

Small molecular weight NTs

36
Q

What are the post-synaptic effects of neuropeptides?

A

Excitatory and inhibitory

37
Q

What are the precursors for neuropeptides?

A

AAs

38
Q

What is the removal mechanism for neuropeptides?

A

Proteases

39
Q

What is the post-synaptic effects of endocannabinoids?

A

Inhibits inhibition

40
Q

What are the precursors for endocannabinoids?

A

Membrane lipids

41
Q

What is the removal mechanism for endocannabinoids?

A

Hydrolysis

42
Q

What are the post-synaptic effects of NO?

A

Excitatory and inhibitory

43
Q

What is the precursor for NO?

A

Arginine

44
Q

What is the removal mechanism for NO?

A

Spontaneous oxidation

45
Q

Where are small molecule NTs synthesised?

A

In the nerve terminal

46
Q

Small molecule NTs mediate very slow synaptic action (T/F?)

A

FALSE- they mediate rapid synaptic action

47
Q

Where are neuropeptides synthesised?

A

In the cell body

48
Q

What is the speed of synaptic action of neuropeptides compared to the small molecule NTs?

A

Neuropeptides have slower ongoing synaptic function

49
Q

What is different about the degradation of small molecule NTs and neuropeptides once they a re released from the pre-synaptic membrane?

A

Small molecule NTs are broken down into their precursors which then diffuse back into the cell. Neuropeptides diffuse away from the terminal and are broken down by proteolytic enzymes.

50
Q

What happens when there is a low frequency of stimulation of the nerve?

A

There is a localised increase in Ca concentration, which results in the preferential release of small molecule NTs.

51
Q

What happens when there is a high frequency of stimulation of the nerve?

A

There is a more diffuse increase in Ca concentration, which results in the release of both types of NTs; small molecule NTs in small clear-core vesicles and neuropeptides in large dense core vesicles.

52
Q

What effect does histamine have on the body?

A

Histamine results in a strong vasodilation, which results in a decrease in BP.

53
Q

What is the difference between ionotropic and metabotropic receptors?

A

Ionotropic receptors are ligand-gated ion channels, and work very rapidly, about 0.1ms.
Metabotropic channels are G protein-coupled receptors, and are slower, taking about 400ms (in the heart).

54
Q

All skeletal muscles are cholinergic in response and have direct cholinergic neurons innervating them. (T/F?)

A

TRUE

55
Q

Dopamine is capable of activating both G-protein coupled (metabotropic) and ionotropic receptors. (T/F?)

A

FALSE- Dopamine acts EXCLUSIVELY by activating G-protein coupled (metabotropic) receptors.

56
Q

What happens to excess dopamine?

A

It is deaminated by MAO in both the PRE and POST-synaptic membrane

57
Q

What type of receptor are ALL of the histamine receptors?

A

G-protein linked

58
Q

Of the three receptor types that are recognised for ATP, how many are G-protein linked?

A

Two- one is ionotropic

59
Q

Only one neuropeptide can be released from a single vesicle. (T/F?)

A

FALSE- more than one NP may be released from a single vesicle

60
Q

What makes a prepropeptide turn into a propeptide?

A

A prepropeptide has a signal sequence on the end, and once this is cleaved it becomes a propeptide.

61
Q

Propeptides can give rise to more than one peptide NT. (T/F?)

A

TRUE

62
Q

Nicotinic receptors are ionotropic ACh receptors (T/F?)

A

TRUE

63
Q

How many subtypes of muscarinic receptors (mAChR) are there?

A

5

64
Q

Where are the mAChR expressed?

A

the striatum and other forebrain regions.
These inhibit dopamine mediated motor effects

65
Q

Glutamate can cross the B/B barrier. (T/F?)

A

FALSE- it must synthesised locally from mitochondrial conversion alpha-ketoglutarate (which comes from the CAC)

66
Q

What does EAATs stand for?

A

Excitatory Amino Acid Transporters

67
Q

What is the function of EAATs and where are they located?

A

They are located on the membranes on both neurons and glial cells. They mediate delivery and uptake of glutamine from glial cells to neurons

68
Q

What is VGLUT and what is its function?

A

VGLUT is a vesicular glutamate transporter- which loads glutamate into neuronal vesicles

69
Q

The NMDA (N-methyl-D-aspartate) is an ionotropic receptor at which glutamate is excitatory. (T/F?)

A

TRUE

70
Q

Where is GABA most common?

A

Local circuit interneurons and cerebellum

71
Q

GABA is removed from the synaptic cleft by specific transporters known as………?

A

GAT- GABA transporter

72
Q

GABA is loaded into neuronal vesicles by which transporter?

A

VIATT- Vesicular Inhibitory Amino Acid Transporter

73
Q

There are three types of GABA receptors, GABAa, GABAb and GABAc. Which two are ionotropic?

A

A and C

74
Q

Which G protein links the GABAb receptor?

A

GI/O

75
Q

The beta gamma subunit of the GABAb receptor blocks two Ca channels, and activates KIR3.1, which does what?

A

The opening of the KIR3.1 means K rushes in and brings the potential further away from the threshold. It causes hyperpolarisation of the post-synaptic membrane.

76
Q

The glycine receptor is a gated channel, gated by which ion?

A

Cl-

77
Q

NO is made by what enzyme?

A

NOS- NO synthase

78
Q

NO had a rapid offset. What happens to it?

A

It is quickly oxidised or bound to Hb

79
Q

How is NO modulated?

A

By regulating NOS function

80
Q

NOS has different isoforms. (T/F?)

A

TRUE

81
Q

NO is not limited to synapses, as it can diffuse between cells. (T/F?)

A

TRUE