In:
Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 98, No. 20 ( 2001-09-25), p. 11680-11685
Abstract:
Synaptotagmin I is a synaptic vesicle-associated protein essential
for synchronous neurotransmission. We investigated its impact on the intracellular Ca 2+ -dependence of large dense-core vesicle
(LDCV) exocytosis by combining Ca 2+ -uncaging and membrane
capacitance measurements in adrenal slices from mouse synaptotagmin I null mutants. Synaptotagmin I-deficient chromaffin cells displayed
prolonged exocytic delays and slow, yet Ca 2+ -dependent
fusion rates, resulting in strongly reduced LDCV release in response to short depolarizations. Vesicle recruitment, the shape of individual
amperometric events, and endocytosis appeared unaffected. These findings demonstrate that synaptotagmin I is required for rapid, highly
Ca 2+ -sensitive LDCV exocytosis and indicate that it
regulates the equilibrium between a slowly releasable and a readily releasable state of the fusion machinery. Alternatively, synaptotagmin
I could function as calcium sensor for the readily releasable pool, leading to the destabilization of the pool in its absence.
Type of Medium:
Online Resource
ISSN:
0027-8424
,
1091-6490
DOI:
10.1073/pnas.201398798
Language:
English
Publisher:
Proceedings of the National Academy of Sciences
Publication Date:
2001
detail.hit.zdb_id:
209104-5
detail.hit.zdb_id:
1461794-8
SSG:
11
SSG:
12
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