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LCRS Neuroscience and Mental Health > neurotransmitters > Flashcards

neurotransmitters Flashcards

neurotransmitters: define the components required for neurotransmitter release, explain the difference between excitatory and inhibitory transmission, identify mechanisms of termination of neurotransmitter action at the synapse, and explain the clinical application of synaptic modulation (for example GABA and epilepsy)

1
Q

properties of synaptic transmission

A

rapid timescale (2ms), diversity, adaptability, plasticity, learning and memroy

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2
Q

3 stages of synpatic transmission pathway

A

transmitter released from 1st cell → synaptic activation of 2nd cell → signal integration and signal conduction by 2nd cell

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3
Q

pathway of action potential in neurone

A

dendrites on spines → soma → axon → nerve endings/terminals

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4
Q

what happens at dendrites

A

information reception

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5
Q

what happens in the soma

A

integration of signals

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6
Q

what happens in the axon

A

rapid transfer of action potential

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7
Q

what happens at nerve terminals

A

synapse onto next body using neurotransmitter release

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8
Q

main components of synapse

A

presynaptic nerve ending, synaptic cleft, postsynaptic region (dendrite/soma)

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9
Q

how large is the synaptic cleft

A

20-100nm

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10
Q

synaptic pathway process

A

action potential reaches presynaptic terminal → causes depolarisation → Na+ influx → K+ outflux → Ca2+ voltage-gated channels open → Ca2+ influx → synaptic vesicles containing neurotransmitters to fuse with membrane → neurotransmitters released by exocytosis → diffuse across synaptic cleft → bind to receptors on postsynaptic region → cause depolarisation → new action potential generated → neurotransmitters removed by transporter into cytosol → Na+/K+ balance restored by Na+/K+ ATPase pump

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11
Q

why are there lots of mitochondria in the presynaptic terminal

A

lots of energy required to produce and release neurotransmitters

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12
Q

is the synapse symmetrical or asymmetrical

A

asymmetrical

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13
Q

properties of neurotransmitters

A

enormous diversity in variety of transmitters and receptors, mediate or slow effects, vary in abundance

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14
Q

what makes up neurotransmitters

A

amino acids, amines, neuropeptides

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15
Q

examples of amino acid neurotransmitters

A

glutamate, GABA, glycine

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16
Q

properties of glutamate

A

most important and potent

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17
Q

what is GABA

A

major inhibitory transmitter in CNS

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18
Q

examples of amine neurotransmitters

A

noradrenaline, dopamine

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19
Q

example of neuropeptide neurotransmitters

A

opioid peptides

20
Q

essential components of synaptic transmission

A

restricted to specialised asymmetric synapse, fast, Ca2+ influx essential, synaptic vesicles as source of neurotransmitter

21
Q

how does rapid release occur

A

synaptic vesicles filled with neurotransmitter and docked in synaptic zone “primed” → Ca2+ influx activates Ca2+ sensor in protein complex → interaction between synaptic vesicle and synaptic membrane proteins allow rapid response → exocytosis → neurotransmitter endocytosis → restart

22
Q

what do neurotoxins such as tetanus target

A

vesicular proteins

23
Q

components required for neurotransmitter release

A

transmitter containing vesicles to be docked on presynaptic membrane, protein complex formation between vesicle, membrane and cytoplasmic proteins (enable docking and rapid response), ATP and vesicle recycling

24
Q

receptors on postsynaptic membrane

A

ion channel and G-protein coupled

25
Q

relative speed and function of ion channel receptors

A

fast; mediate all fast excitatory and inhibitory transmission

26
Q

relative speed and function of G-protein coupled receptors

A

slow; activate effector: enzyme (e.g. adenyl cyclase) or channels (e.g. Ca2+)

27
Q

ion channel receptor in CNS

A

GABA

28
Q

ion channel receptor in NMJ (neuromuscular junction)

A

acetylcholine

29
Q

G-protein coupled receptor in CNS and PNS

A

acetylchonline, dopamine, noradrenaline, 5HT, neuropeptides

30
Q

properties of ion channel-linked receptors

A

rapid activation, diversity and rapid information flow, multiple subunit combinations for distinct functional properties

31
Q

GLUR

A

excitation (Na+ influx - depolarise membrane)

32
Q

GABAR

A

inhibitory (Cl- influx - hyperpolarise membrane)

33
Q

where is GLUR usually found

A

dendrites

34
Q

where is GABAR ususally found

A

soma so acts downstream of GLUR

35
Q

excitatory receptor (e.g. GLUR)

A

depolarises membrane

36
Q

inhibitory receptor (e.g. GABAR)

A

hyperpolarises membrane

37
Q

glutamate receptors

A

AMPA and NMDA

38
Q

AMPA receptor

A

Na+ influx; only acts on cell which has already been depolarised; majority of fast excitatory synapses

39
Q

NMDA receptor

A

Na+ and Ca2+ influx; Ca2+ modifies recepor, activates protein synthesis which modifies synapse formation; slow component of excitatory transmission; serve as coincidence detectors which underlie learning mechanisms

40
Q

excitatory synapse mediated by glutamate and inhibition

A

mediated by depolarising membrane; EAAT (transporter) takes glutamate into glial cell; conversion of glutamate to glutamine by glutamine synthetase

41
Q

what does abnormal cell firing associated with excess glutamate in synapse lead to

A

epileptic seizures

42
Q

epilepsy characterisation

A

recurrent seizures due to abnormal neuronal excitability

43
Q

GABA structure vs glutamate structure

A

GABA is glutamate without COOH group; catalysed by glutamic acid decarboxylase

44
Q

inhibitory synapse mediated by GABA and inhibition

A

mediated by hyperpolarising membrane; GAT (transporter) takes GABA into glial cell; conversion of GABA to succinate semialdehyde by GABA-T

45
Q

treating epilepsy

A

drugs dampen down excitatory activity and target pentameric organisation of GABA, enhancing enhance transmission and influx of Cl- (e.g. increases frequency of Cl- channel opening)

LCRS Neuroscience and Mental Health (38 decks)

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