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Biomembranes > Transmitter Release > Flashcards

Transmitter Release Flashcards

- Appreciate how electrophysiological, microscopy and biochemical techniques can be used to investigate the release of a neurotransmitter at a synapse - Describe key experiments used to investigate the role of vesicles in neurotransmitter release - Understand the role of key synaptic proteins in neurotransmitter release - Know how to determine the effects of particular drugs and toxins on synaptic transmission

1
Q

Where are nicotinic receptors expressed

A

brain and spinal cord

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2
Q

Speed of action potentials

A

up to 120 metres/sec

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3
Q

Role of neurotransmitters

A
  • carry signal across the synaptic cleft
  • cause excitation or inhibition
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4
Q

Steps of synaptic transmission

A

1) presynaptic AP
2) calcium influx via voltage-gated calcium channels
3) vesicular transmitter release
4) action of transmitter-gated ion channels
5) postsynaptic depolarisation of cation conducting transmitter-gated ion channels activate postsynaptic voltage-gated ion channels & initiate AP

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5
Q

How is fast synaptic transmission mediated

A

transmitter-gated ion channels

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6
Q

What are transmitter-gated ion channels (cys-loop family)

A
  • e.g. nAChR
  • integral ion channel
  • agonist binding to receptor induces rapid conformational change to open channel
  • selective for certain ions
  • extremely rapid signalling
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7
Q

How are nAChRs identified on alpha-bungarotoxin at the NMJ

A

red fluorescent, binds irreversibly

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8
Q

Origins of a mepp

A
  • results from a spontaneous release of just a single neurotransmitter packet
  • at the end plate region vesicles
  • open simultaneously -> sodium flux (depolarisation, AP)
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9
Q

How can we use electron microscopy to study synapses

A

reveal vesicles at the synapse in exocytosis

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10
Q

Action of Vesamicol

A
  • inhibits vesicular uptake of ACh and decreases amplitude of mepps
  • response to iontophoretically applied ACh remains unchanged by vesamicol, suggesting that the decrease in the amount of ACh in the vesicle is the reason for the decrease of mepp amplitude
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11
Q

How alpha-LTX influences transmitter release

A
  • depletion of vesicles
  • inhibition of endocytosis
  • distended terminal paralysis
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12
Q

Mechanism of alpha-LTX

A
  • involving both calcium dependent and independent pathways
  • binds to specific presynaptic receptors (Neurexin and Latrophilin)
  • toxin forms a cation (Na/Ca) conducting pore/channel
  • 2 specific binding sites on presynaptic nerve
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13
Q

Steps of recycling synaptic vesicles

A
  1. Budding of endosome
  2. Docking of neurotransmitter
  3. Priming vesicle for release
  4. Fusion of vesicle to membrane
  5. Endocytosis via “Kiss and Run” / “Clathrin pathway”)
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14
Q

Calcium role in neurally-evoked neurotransmitter release

A
  • localised calcium entry via coltage-gated calcium channels
  • calcium triggers vesicle fusion
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15
Q

Technical issue for studying nerve stimulation at NMJ

A

nerve stimulation causes muscle contraction which results in breakage of glass microelectrode (use high Mg / low Ca buffered solution)

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16
Q

Why is it beneficial to use high Mg / low Ca extracellular solution to measure nerve stimulation

A

it brings the epp to below threshold for AP firing

17
Q

Describe what is meant by neurotransmitter release at the NMJ is quantal

A
  • amplitude of smallest event = amplitude of mepp
  • stimulating multiple times provides varying responses depending on conditions -> shows repetitive peaks that are multiples of each other
18
Q

Define the quantal content

A

QC = mean epp amplitude / mean mepp amplitude

19
Q

Factors influencing the amplitude of the mepp

A
  • number of nicotinic receptors
  • amount of ACh stored in each vesicle
20
Q

How is a muscle contraction stimulated?

A

mepps summate to give epp, which, if large enough, exceeds threshold and initiates an AP, causing muscle contraction

21
Q

How is neuronal excitation stimulated in the CNS

A
  • miniature excitatory postsynaptic potentials (mEPSPs) summate to produce excitatory post synaptic potential (EPSP), causing neuronal excitation
22
Q

Mechanism of action of dendrotoxin

A
  • works presynaptically
  • large increase in EPP amplitude
  • large increase in QC
  • no change MEPP
  • blocks voltage-gated potassium channels
  • limits repolarisation by potassium channels (control duration of AP)
  • longer AP, increased Ca influx, increase vesicle release
23
Q

Mechanism of action of Tubocurarine

A
  • works postsynaptically
  • competitive antagonist for nAChRs
  • reduces EPP below threshold
  • reduces MEPP
  • no change QC
  • stops skeletal muscle contracting (skeletal neuromuscular blocker)
24
Q

Mechanism of action of botulinum toxin

A
  • works presynaptically
  • decreases QC
  • decreases EPP
  • no change MEPP
  • decrease neurally-evoked ACh release via 4 steps
25
Q

4 steps of Botulinum toxin vesicular inhibiton

A
  1. Attachment onto cholinergic presynaptic nerve
  2. Toxin enters by endocytosis
  3. Light chain in cytoplasm
  4. Proteolytic cleavage of synaptobrevin
26
Q

Role of light chain

A

acts like protease and cleaves important components of proteins expressed on vesicles that are essential for vesicular fusion

27
Q

What is synaptotagmin (VAMP)

A
  • calcium sensor
  • binds calcium cooperatively and undergoes conformational change
  • “knock-out” mice calcium-dependent transmitter release is impaired
  • Drosophila synaptotagmin mutants exhibit impaired release and impaired sensitivity to calcium
28
Q

Describe a simple model of vesiclar release

A

1) docking: complex of synaptobrevin, syntaxin, and SNAP 25 form to bring vesicle into the active zone adjacent to calcium channel
2) priming: synaptotagmin is recruited to the complex
3) fusion: calcium influx triggers fusion and transmitter release

29
Q

Role of magnesium in neurally-evoked transmitter release

A
  • magnesium blocks the voltage-gated calcium ion channel and allows us to study neurally-evoked transmitter release
  • fusing solution of high mg and low ca reduces epps

Biomembranes (12 decks)

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