Flashcards
Neurotransmitter release
Cards in this deck (19)
- 1Describe the steps of fast synaptic transmission1) Action potential.
2) Ca2+ influx via Ca2+ channels.
3) Vesicular transmitter release.
4) Activation of transmitter-gated
ion channels.
5) Activation of voltage-gated
ion channels. - 2What mediates fast synaptic transmission?Fast synaptic transmission is mediated by
transmitter-gated ion channels - 3Describe the main features of the cys-loop superfamily of transmitter-gated ion channelsEg. The nicotinic acetylcholine receptor (nAChR).
integral ion channel
agonist binding to the receptor induces a rapid conformational change to open the channel
the channel is selective for certain ions.
signalling is extremely rapid (milliseconds). - 4What is the action of Vesamicol on ACh vesicular uptake and the amplitude of mepps?Vesamicol – inhibits vesicular uptake of ACh &
consequently decreases the amplitude of mepps.
Theoretically, the decrease
in amplitude could result
from the drug:
1) inhibiting the
post-synaptic receptors or by
2) Decrease the amount of ACh
in the vesicle.
However, the response to
iontophoretically applied ACh.
remains unchanged by vesamicol
suggesting mechanism 2. - 5What is the effect of black widow spider venom (alpha-LATROTOXIN) on neurotransmitter release?BLACK WIDOW SPIDER VENOM (a-LATROTOXIN) INFLUENCES SPONTANEOUS TRANSMITTER RELEASE
Causes massive release of ACh vesicles which causes many mepps and muscle spasms
After depletion of vesicles there is inhibition of endocytosis and distended terminal paralysis - 6What is the effect of 4-aminopyridine (4-AP)?4-aminopyridine (4-AP) increases
evoked neurotransmitter release - 7What ion extracellular concentrations reduce the epp to below the threshold for firing an AP?A high Mg2+ low Ca2+ extracellular solution reduces the epp to below the threshold for firing an action potential.
- 8How is quantal content (QC) calculated?QC = mean EPP amplitude (mV) / mean MEPP amplitude (mV)
- 9How does vesicle release lead to a muscle contraction?Release of a vesicle gives a “quanta” of transmitter.
Each quanta gives rise to a miniature end plate potential (mepp) via activation of nicotinic ACh receptors.
Mepps summate to give an end plate potential (epp), which, initiates an action potential and leads to muscle contraction. - 10How do mEPSPs in the CNS cause neuronal excitation?Similarly in the CNS, glutamate receptor mediated miniature excitatory postsynaptic potentials (mEPSPs) summate to produce an EPSP and leads to neuronal excitation.
- 11How do mIPSPs cause neuronal inhibition?GABAA receptor mediated miniature inhibitory postsynaptic potentials summate to produce an IPSP and leads to neuronal inhibition.
- 12What is the effect of dendrotoxin (4-aminopyridine) on quantal content?Dendrotoxin, or 4-aminopyridine increase quantal content.
Dendrotoxin, or 4-AP blocks voltage-gated K+ channels -> prolonged action potential->
(↑ Ca2+ influx -> ↑ release)
EPP ↑, MEPP no change = QC ↑. - 13How does tubocurarine effect neurotransmitter release?Tubocurarine: EPP decrease, MEPP decrease = QC no change.
Tubocurarine acts postsynaptically
to block the nicotinic ACh receptors. - 14How does botulinum toxin affect synapses?Botulinum Toxin: decrease EPP, MEPP no change = decrease QC .
It acts pre-synaptically to decrease neurally
evoked ACh release. - 15What are the three modes of neurotransmitter release?Synchronous-evoked release
Asynchronous-evoked release
Spontaneous release - 16Describe the mechanism of botulinum toxin inhibitionBotulinum toxin inhibits action potential evoked vesicular release.
Synaptobrevin- a vesicle associated membrane protein (VAMP).
Synaptobrevin “knock-out” mice: a near complete loss of Ca2+-dependent release that is evoked in tight synchrony with presynaptic action potentials. By contrast, the majority of spontaneous & asynchronous release (loosely coupled to stimulation) is left intact.
1. Attachment of light and heavy chain
2. Toxin enters by endocytosis
3. Light chain in the cytoplasm
4. Proteolytic cleavage of synaptobrevin - 17What is the evidence for synaptotagmin being a VAMP (a vesicle associated membrane protein that may be a Ca2+ sensor)1) It binds Ca2+ cooperatively & then undergoes a conformational change.
2) In synaptotagmin “knock-out” mice Ca2+-dependent transmitter release is impaired.
3) Drosophila synaptotagmin mutants exhibit impaired release & sensitivity to Ca2+.
4) Transmitter release at the squid giant synapse is blocked by presynaptic injection of a 20 amino acid synaptotagmin peptide. - 18What is the effect of synaptotagmin on neurotransmitter release?Synaptotagmin decreases transmitter release therefor decreasing MEPP
- 19Give an overview of vesicular release1) Docking: A complex of synaptobrevin, syntaxin & SNAP 25
forms to bring the vesicle into the active zone adjacent
to the Ca channel.
2) Priming: Synaptotagmin is recruited to the complex.
3) Fusion: Calcium influx triggers fusion & transmitter release.
(synaptotagmin and synaptobrevin are Vesicle Associated Membrane Proteins (VAMPs))
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- Biomembranes Flashcards on Neurotransmitter release, created by Megan MacLeod on 14/06/2019.
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- Megan MacLeod
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