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OCB > OCB03-2008 Neurotransmitters 1: Glutamate, GABA & Acetylcholine > Flashcards

OCB03-2008 Neurotransmitters 1: Glutamate, GABA & Acetylcholine Flashcards

1
Q

What is the firing of an action potential determined by?

A

The number of excitatory and inhibitory synaptic inputs

The strength of the individual inputs

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2
Q

How do synaptic neurons inhibit neurons?

A

Hyperpolarisation

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3
Q

How do synaptic neurons excite neurons?

A

Depolarisation

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4
Q

what is glutamate?

A

A major excitatory neurotransmitter in the CNS

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5
Q

What are the glutamatergic pathways involved in?

A

Involved in portico-cortical pathways
Pathways between the cortex and thalamus
Involed in pathways between the cortex and striatum

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6
Q

What physical processes are glutamate involved in?

A

Emotions, memory and cognition

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7
Q

What psychiatric conditions are glutamate associated with?

A

Depression
Anxiety
Drug addiction
Schizophrenia

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8
Q

How does glutamate access the brain?

A

It does not cross the BBB so the brain cannot supply glutamate via circulation
Instead is is synthesised by the metabolism of glucose and from glutamine synthesised in astrocytes

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9
Q

How does glutamate work as a neurotransmitter?

A

Glutamine enters the presynaptic neurone where it is converted into the glutamate via glutaminase
Influx of Ca2+ causes the synaptic vesicles to fuse with the membrane and release glutamate
Glutamate binds to post synaptic receptors and diffuses out of the synaptic cleft and binds to glutamate transporter on the astrocyte
Glutamate is converted back to glutamine via glutamate synthase
Glutamine exits the astrocyte via the glutamine transporter init the ECS

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10
Q

What are the 2 types of glutamate receptor?

A

Ionotropic and Metabatrophic

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11
Q

What are the glutamate ionotropihic subtypes?

A

NMDA
AMPA
Kainate

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12
Q

What type of channel is Metabotropic?

A

GPCR

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13
Q

What is AMPA and Kainate transmission like?

A

Fast synaptic current with fast decay

Influx Na+ ions cause depolarisation

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14
Q

What is a blockage of AMPA receptors likely to cause?

A

Inhibitory effect on CNS

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15
Q

What is NMDA transmission like?

A

Slower onset and slower decay

Higher affinity for glutamate

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16
Q

What is a blockage of NMDA likely to cause?

A

Effects on behaviour and memory

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17
Q

Why does NMDA have a slower response?

A

It has a higher affinity for glutamate
Mg2+ blocks the channel at less than -50mV
Depolarisation of AMPA removes Mg2+ block

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18
Q

Why does NMDA continuously active after glutamate concentration is 0?

A

NMDA has a high affinity for glutamate

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19
Q

How to pre-synaptic glutamate metabatropic receptors work?

A

Inhibits Ca voltage gated channels so there is less calcium influx into the pre-synaptic terminal and so reduces the amount of neurotransmitter released form other terminals

20
Q

How to post-synaptic glutamate metabatropic receptors work?

A

Modifies the activity of K+ channels so changes the number if action potentials
Modulating the excitability of a neurone

21
Q

What is the consequence of excess glutamate?

A

Excitotoxicity and ischaemic cell death

22
Q

What is GABA?

A

Major inhibitory neurotransmitter

23
Q

What diseases are associated with loss of GABA?

A

Epilepsy
Huntington’s disease
Uncontrollable movements

24
Q

How is GABA formed?

A

Formed from glutamate by acton of glutamic acid decarboxylase

25
Q

How does GABA work as a neurotransmitter?

A

GABA is transported into synaptic vesicles then released during an action potential
It diffuses across the synaptic cleft and interacts with receptors
It diffuses back into the astrocyte via GABA transporters

26
Q

What are the two GABA receptors?

A

Ionotrophic GABAA receptors

Metabotropic GABAB receptors

27
Q

Where are GABAA receptors found?

A

Post-synaptically

28
Q

Where are GABAB receptors found?

A

Pre and post synaptically

29
Q

How do GABAA mediate inhibition?

A

They allow chloride ions to flow into the cell which:
Hyperpolarises the neuron
Inhibits depolarisation

30
Q

What can block of GABAA cause?

A

Convulsions (involuntary contraction of muscles)

31
Q

What drugs enhance opening on GABAA chloride channels?

A

ethanol
Benzodiazepines
GA

32
Q

How do GABAB receptors work?

A

Coupled to Gi so when activated inhibits adenylate cyclase

33
Q

Which GABA receptors is longer-lasting?

A

GABAB

34
Q

What does presynaptic inhibition cause?

A

Inhibiton of voltage-gated Ca2+ channels which decreases transmitter release

35
Q

What does post-synaptic inhibition cause?

A

Increased opening of K+ channels which reduced firing of action potentials

36
Q

How is acetylcholine formed?

A

Acetyl and choline combine via choline acetyltransferase to form acetylcholine

37
Q

How is acetylcholine broken down?

A

It is hydrolysed by acetylcholinesterase and choline is taken up pre-synaptically

38
Q

What receptors do ACh act on?

A

Nicotinic and muscarinic

39
Q

What subunits make up the nicotinic receptor?

A

2 alpha

3 beta

40
Q

Which subunit of nicotinic receptor does acetylcholine bind to?

A

alpha

41
Q

What occurs when ACh binds to a nicotinic receptor?

A

Causes a conformational change and increased permeability to Na+, K+ and Ca2+
K flows out and Na and Ca flow in

42
Q

What is the presynaptic effect of ACh binding to the nicotinic receptor?

A

Neurotransmitter release

43
Q

What is the postsynaptic effect of ACh binding to the nicotinic receptor?

A

fast excitation and depolarisation

44
Q

How do M1, M3 and M5 work?

A

They are linked to phospholipase C activation which controls calcium release

45
Q

How do M2 and M4 work?

A

Inhibits adenylate cyclase

OCB (16 decks)

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