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
relative speed and function of ion channel receptors
fast; mediate all fast excitatory and inhibitory transmission
26
relative speed and function of G-protein coupled receptors
slow; activate effector: enzyme (e.g. adenyl cyclase) or channels (e.g. Ca2+)
27
ion channel receptor in CNS
GABA
28
ion channel receptor in NMJ (neuromuscular junction)
acetylcholine
29
G-protein coupled receptor in CNS and PNS
acetylchonline, dopamine, noradrenaline, 5HT, neuropeptides
30
properties of ion channel-linked receptors
rapid activation, diversity and rapid information flow, multiple subunit combinations for distinct functional properties
31
GLUR
excitation (Na+ influx - depolarise membrane)
32
GABAR
inhibitory (Cl- influx - hyperpolarise membrane)
33
where is GLUR usually found
dendrites
34
where is GABAR ususally found
soma so acts downstream of GLUR
35
excitatory receptor (e.g. GLUR)
depolarises membrane
36
inhibitory receptor (e.g. GABAR)
hyperpolarises membrane
37
glutamate receptors
AMPA and NMDA
38
AMPA receptor
Na+ influx; only acts on cell which has already been depolarised; majority of fast excitatory synapses
39
NMDA receptor
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
excitatory synapse mediated by glutamate and inhibition
mediated by depolarising membrane; EAAT (transporter) takes glutamate into glial cell; conversion of glutamate to glutamine by glutamine synthetase
41
what does abnormal cell firing associated with excess glutamate in synapse lead to
epileptic seizures
42
epilepsy characterisation
recurrent seizures due to abnormal neuronal excitability
43
GABA structure vs glutamate structure
GABA is glutamate without COOH group; catalysed by glutamic acid decarboxylase
44
inhibitory synapse mediated by GABA and inhibition
mediated by hyperpolarising membrane; GAT (transporter) takes GABA into glial cell; conversion of GABA to succinate semialdehyde by GABA-T
45
treating epilepsy
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)