Synaptic vesicle exocytosis
Molecular mechanisms and clinical implications
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Chemical synapses are the main mechanism of communication in the nervous system. At the presynaptic terminal, neurotransmitters are packaged into synaptic vesicles (SVs); when an action potential opens presynaptic voltage-gated Ca2+ channels, the neurotransmitters are released by Ca2+-triggered exocytosis into the synaptic cleft to activate postsynaptic receptors. SV exocytosis is restricted to the small section of the presynaptic plasma membrane called the active zone, which contains clustered Cav2 (P/Q- and N-type) voltage-gated Ca2+ channels.
GLOSSARY
- BoNT=
- botulinum neurotoxin;
- CaM=
- calmodulin;
- CSP=
- cysteine-string protein;
- Munc-13=
- mammalian uncoordinated–13;
- NSF=
- N-ethylmaleimide sensitive factor;
- RIM=
- Rab-3 interacting molecules;
- RIM-BP=
- RIM binding protein;
- SNAP=
- soluble NSF-attachment protein;
- SNARE=
- SNAp-REceptor;
- SV=
- synaptic vesicle;
- SV2=
- synaptic vesicle glycoprotein–2;
- synprint=
- synaptic protein interaction;
- TeNT=
- tetanus neurotoxin
Footnotes
Go to Neurology.org for full disclosures. Funding information and disclosures deemed relevant by the author, if any, are provided at the end of the article.
- Received March 24, 2013.
- Accepted in final form March 24, 2013.
- © 2013 American Academy of Neurology
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