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Module 202 Neuroscience & behaviour > T1 L6 Chemicals in the brain > Flashcards

T1 L6 Chemicals in the brain Flashcards

1
Q

How is the pool of vesicles above the active zone anchored to the cytoskeleton?

A

By synapsin

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2
Q

What activates calcium calmodulin activated kinase II?

A

Calcium ions

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3
Q

What does calcium calmodulin activated kinase II do?

A

Phosphorylates synapsin

P-synapsin can no longer bind to the cytoskeleton so vesicles dock to the active zone

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4
Q

What does the SNARE complex do?

A

It docks vesicles to the plasma membrane at the active zone

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5
Q

Describe the 4 steps of exocytosis during neurotransmitter release

A

1) Vesicle docks
2) SNARE complexe form to pull membranes together
3) Entering calcium binds to synaptotagmin
4) Calcium-bound synaptotagmin catalyses membrane fusion by binding to SNAREs and the plasma membrane

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6
Q

What does the botulinum toxin do?

A

Decreases neuromuscular transmission of acetylcholine

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7
Q

Where does botox come from?

A

Clostridium botulinum

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8
Q

Where do tetanus toxins come from?

A

Clostridium Tetani

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9
Q

What does botox do?

A

Acts directly at neuromuscular junction

Muscles lose all input so become permanently relaxed

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10
Q

What does the tetanus toxin do?

A

Inhibits the release of Glycine and GABA at inhibitory neurons
Results in dis-inhibition of cholinergic neutrons
Causes permanent muscle contraction

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11
Q

What diseases affect the presynaptic terminal?

A 
Congenital myasthenic syndromes
LEMS
Cognitive disorders
Botulinum & tetanus toxins
Latrotoxin
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12
Q

How does LEMS affect the presynaptic terminal?

A

Attacks presynaptic calcium channels

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13
Q

How does congenital myasthenic syndrome affect the presynaptic terminal?

A

Results in impaired vesicle recycling

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14
Q

How does latrotoxin affect the presynaptic terminal?

A

Triggers vesicle fusion

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15
Q

How do cognitive disorders affect the presynaptic terminal?

A

They impair transsynaptic signalling

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16
Q

How are vesicular transporters powered by proton gradients?

A

ATPase proton pump loads up vesicles with H+

Makes vesicles acidic

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17
Q

How are plasma membrane transporters powered by electrochemical gradients?

A

Na concentration is higher outside & K is higher inside

Glutamate is cotransported with 2 Na+

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18
Q

What are astrocytes?

A

A type of glial cell with extensions that wrap around the gaps or synapses between neurons

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19
Q

What are the categories of neurotransmitters?

A

Amino acids
Monoamines
Acetylcholine
Neuropeptides

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20
Q

Where are neuropeptides synthesised?

A

In the cell soma & transported to the terminal

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21
Q

Where are neuropeptides stored?

A

In secretory granules

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22
Q

What stimulates a release of neuropeptides?

A

A global increase in calcium ions

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23
Q

Where are amino acids, monoamines & acetylcholine synthesised & stored?

A

Synthesised locally in presynaptic terminal

Stored in synaptic vesicles

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24
Q

What stimulates a release of amino acids, monoamines or acetylcholine?

A

A local increase in calcium ions

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25
Q

Give an example of a fast neurotransmitter

A

Amino acids

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26
Q

Give an example of a slow neurotransmitter

A

Neuropeptides

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27
Q

What is a fast neurotransmitter?

A

Stored in synaptic vesicles docked close to a voltage-gated calcium channels in membrane of nerve terminal
Released in short burst when membrane is depolarised

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28
Q

What is a slow neurotransmitter?

A

Stored in separate vesicles further from the membrane

Release is slower as they have to migrate first to the membrane & only occurs when calcium builds up sufficiently

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29
Q

Give an example of an excitatory amino acid transmitter?

A

Glutamate in the CNS

Slightly depolarises postsynaptic cell’s membrane

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30
Q

Give an example of an inhibitory amino acid transmitter?

A

GABA in the brain
Glycine in the spinal cord & brainstem
Slightly hyperpolarises postsynaptic cell’s membrane

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31
Q

Give an example of a modulatory system

A

Serotonergic system

32
Q

What is modulation?

A

Affects large neural networks, cortex, spinal cord, cerebellum
Changes how likely these areas are to be excited

33
Q

What are some functions of the serotonergic system?

A 
Mood
Sleep
Pain
Emotion
Appetite
34
Q

What are the 2 ways glutamate is synthesised?

A

From glucose via the Krebs cycle

From glutamine converted by glutamine into glutamate

35
Q

What do vesicular glutamate transporters do?

A

Load & store glutamate into vesicles

36
Q

How is glutamate taken back up?

A

By excitatory amino acid transporters in the plasma membrane of presynaptic cell & surrounding glia

37
Q

How is glutamate converted to glutamine?

A

By glial cells

Glutamine then transported from the glia back to nerve terminals where it is converted back into glutamate

38
Q

How is GABA synthesised?

A

From glutamate in a reaction catalysed by glutamic acid decarboxylase

39
Q

What do vesicular GABA transporters do?

A

Load & store GABA into vesicles

Gly also uses this transporter

40
Q

How is GABA cleared from the synapse?

A

By reuptake using transporters on glia & neutrons including non-GABAergic neurons

41
Q

What happens if there is too much Glu or too little GABA?

A

Hyper excitability
Epilepsy
Excitotoxicity

42
Q

What happens if there is too much GABA?

A

Sedation / coma

43
Q

What happens in cerebral ischaemia?

A

Metabolic events that retain electrical gradient are abolished
Reversal of Na/K gradient
Transporters release glutamate from cells by reverse operation
Excitotoxic cell death

44
Q

What happens with GHB (date-rape drug)?

A

GABA metabolite that is converted back to GABA
Increases amount of available GABA
Too much leads to unconsciousness & coma

45
Q

What are the 2 types of monoamines?

A

Catecholamines

Indolamines

46
Q

Give some examples of catecholamines

A

Dopamine
Epinephrine
Norepinephrine

47
Q

Give an example of an indolamine

A

Serotonin

48
Q

Describe the path of dopamine synthesis

A

Tyrosine –> dopa –> dopamine –> NE –> epinephrine

49
Q

What do vesicular monoamine transporters do?

A

Load catecholamines into vesicles for storages

50
Q

What does L-DOPA (Levodopa) do?

A

Precursor of dopamine
Used to treat Parkinson’s disease
Dopa decarboxylase converts it into dopamine increasing the pool of releasable transmitter

51
Q

How is catecholamine released?

A

By calcium dependent exocytosis

52
Q

What happens once catecholamine is released?

A

It binds and activates the receptor

53
Q

How is the signal for catecholamine release terminated?

A

By reuptake into the axon terminal by transporters powered by the electrochemical gradient.
Dopamine transporters, norepinephrine transporters

54
Q

What happens to catecholamines in the cytoplasm?

A

They are reloaded back into vesicles
Enzymatically degraded by monoamine oxidases (MAOs)
Inactivated by catechol-O-methyl-transferase (COMT)

55
Q

What effect does amphetamine have on catecholamine?

A

Reverse transporter so pumps out transmitter & blocks uptake (DA & NE)

56
Q

What effect does cocaine & methylphenidate have on catecholamine?

A

(Ritalin) block DA reuptake into terminals

More DA in synaptic cleft - extended action on postsynaptic neuron

57
Q

What effect does selegiline have on catecholamine?

A

MAO inhibitor found in dopaminergic nerve terminals
Prevents degradation of DA allowing more to be released on subsequent activations
Used to treat early-stage PD, depression & dementia

58
Q

What effect does entacopone have on catecholamine?

A

COMT inhibitor

Treatment of PD

59
Q

How is serotonin synthesised?

A

Tryptophan –> 5-hydroxytryptophan –> serotonin

60
Q

Describe serotonin storage, release & reuptake

A

Stored in vesicles
Signal terminated by reuptake by serotonin transporters on presynaptic membrane
Destroyed by MAOs in the cytoplasm

61
Q

What drugs module the release and reuptake of serotonin?

A

Fluoxetine
Fenfluramine
MDMA

62
Q

How does fluoxetine (prozac) affect serotonin?

A

Blocks reuptake of serotonin
SSRI - selective serotonin reuptake inhibitor
Treatment of depression & OCD

63
Q

How does fenfluramine affect serotonin?

A

Stimulates the release of serotonin & inhibits its reuptake
Has been used as an appetite suppressant in the treatment of obesity

64
Q

How does MDMA affect serotonin?

A

(Ecstasy) causes NE & serotonin transporters to run backwards released neurotransmitter into synapse / extracellular space

65
Q

Describe the synthesis of acetylcholine

A

Choline acetyltransferase converts choline & acetyl CoA into acetylcholine

66
Q

What is the function of vesicular acetylcholine transporter?

A

Packages acetylcholine into vesicles

67
Q

What does acetylcholinesterase do?

A

Rapidly degrades acetylcholine in the synaptic cleft.

Choline is then transported back into the presynaptic terminal & converted to acetylcholine

68
Q

Describe the synthesis & secretion of acetylcholinesterase

A

Made by cholinergic neuron

Secreted into synaptic cleft & associated with axonal membrane

69
Q

What do acetylcholinesterase inhibitors do?

A

Block the breakdown of acetylcholine which prolongs its actions in the synaptic cleft

70
Q

Give an example of an acetylcholinesterase inhibitor

A

Neostigmine

71
Q

Describe the properties of neuropeptides

A

Slow transmission
Vary in their methods of synthesis & release from small molecule transmitters
Short polypeptide chains 3-36 amino acids
Over 100 neuropeptides described

72
Q

Describe the process of neuropeptide release & degradation

A

Follow secretory pathway
Not released in same way as small molecule transmitters

1) Dense core vesicle fusion & exocytosis occurs due to global elevations of Ca2+
2) Neuropeptide vesicle membrane is recycled but not refilled
3) Bind to & activate receptor
4) Neuropeptide signalling is terminated by diffusion from site of release & degradation. by proteases in extracellular environment
5) Release is slower than small molecule release & signals may be maintained for longer

73
Q

Describe what happens to nitric oxide

A

1) Nitric oxide is made in postsynaptic neuron by nitric oxide synthase
2) Gas rapidly diffuses from its site of synthesis
3) Activates guanylyl cyclase which makes cGMP
4) Within a few sec of being produced, NO is converted to biologically inactive compound
5) Potentially useful for coordinating activities of multiple cells in a small region

74
Q

How is nitric oxide synthase activated?

A

By the binding of Ca2+ & calmodulin

75
Q

What are endocannabinoids?

A

Small lipids which mostly cause reduced GABA release at certain inhibitory terminals

Module 202 Neuroscience & behaviour (39 decks)

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