Synaptic function is impaired but not eliminated in C. elegans mutants lacking synaptotagmin

Michael L. Nonet, Kiely Grundahl, Barbara J. Meyer, James B. Rand

Research output: Contribution to journalArticlepeer-review

458 Scopus citations

Abstract

Synaptotagmin is an abundant synaptic vesicle-associated protein proposed to be involved in calcium-mediated neurotransmitter release. Our molecular and genetic results demonstrate that, although synaptotagmin is required for the proper function of the presynaptic nerve terminal in C. elegans, some neurotransmitter release persists in synaptogamin mutants. In C. elegans neurons, synaptotagmin is localized to regions known to be rich in synapses and appears to be associated with synaptic vesicles. Mutants defective in the synaptotagmin gene, called snt-1, exhibit severe behavioral abnormalities that are characteristic of deficiencies in synaptic function, including severe locomotion, feeding, and defecation defects. The mutants are defective in exocytosis, since they accumulate acetylcholine, and are resistant to cholinesterase inhibitors, but they nevertheless remain sensitive to cholinergic receptor agonists. In spite of these exocytic defects, snt-1 mutants are capable of coordinated motor movements, indicating that the mutants do not have a complete block of neurotransmitter release.

Original languageEnglish
Pages (from-to)1291-1305
Number of pages15
JournalCell
Volume73
Issue number7
DOIs
StatePublished - Jul 2 1993

Fingerprint

Dive into the research topics of 'Synaptic function is impaired but not eliminated in C. elegans mutants lacking synaptotagmin'. Together they form a unique fingerprint.

Cite this