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Synaptotagmin I‐ and II‐deficient PC12 cells exhibit calcium‐independent, depolarization‐induced neurotransmitter release from synaptic‐like microvesicles
Author(s) -
Bauerfeind Rudolf,
Jelinek Ruth,
Huttner Wieland B.
Publication year - 1995
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(95)00419-a
Subject(s) - synaptotagmin 1 , depolarization , exocytosis , synaptotagmin i , neurotransmitter , microvesicles , stx1a , microbiology and biotechnology , calcium , chemistry , secretion , synaptic vesicle , neurosecretion , biophysics , biology , endocrinology , syntaxin , biochemistry , vesicle , receptor , membrane , microrna , organic chemistry , gene
Synaptotagmin I‐ and II‐deficient PC12 cells (ShojiKasai et al. [1]) were used to compare the role of this protein in the calcium‐dependent exocytosis of secretory granules and synaptic‐like microvesicles (SLMVs). While neither catecholamine nor protein secretion from secretory granules were altered, the depolarization‐induced acetylcholine release from SLMVs was no longer calcium‐dependent. We propose that within the exocytotic process of SLMVs, there exist two depolarization‐induced steps. One is calcium‐dependent and no longer present in synaptotagmin I‐ and II‐deficient cells. The other is induced by depolarization, does not require calcium, and suffices to trigger neurotransmitter release from SLMVs in synaptotagmin I‐ and II‐deficient PC12 cells.