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EMBO J. 2006 May 17;25(10):2039-50. Epub 2006 Apr 27.

Genetic analysis of synaptotagmin 2 in spontaneous and Ca2+-triggered neurotransmitter release.

Author information

1
Department of Molecular Genetics, Center for Basic Neuroscience, Howard Hughes Medical Institute, UT Southwestern Medical Center, Dallas, TX 75390-9111, USA.

Abstract

Synaptotagmin 2 resembles synaptotagmin 1, the Ca2+ sensor for fast neurotransmitter release in forebrain synapses, but little is known about synaptotagmin 2 function. Here, we describe a severely ataxic mouse strain that harbors a single, destabilizing amino-acid substitution (I377N) in synaptotagmin 2. In Calyx of Held synapses, this mutation causes a delay and a decrease in Ca2+-induced but not in hypertonic sucrose-induced release, suggesting that synaptotagmin 2 mediates Ca2+ triggering of evoked release in brainstem synapses. Unexpectedly, we additionally observed in synaptotagmin 2 mutant synapses a dramatic increase in spontaneous release. Synaptotagmin 1-deficient excitatory and inhibitory cortical synapses also displayed a large increase in spontaneous release, demonstrating that this effect was shared among synaptotagmins 1 and 2. Our data suggest that synaptotagmin 1 and 2 perform equivalent functions in the Ca2+ triggering of action potential-induced release and in the restriction of spontaneous release, consistent with a general role of synaptotagmins in controlling 'release slots' for synaptic vesicles at the active zone.

PMID:
16642042
PMCID:
PMC1462977
DOI:
10.1038/sj.emboj.7601103
[Indexed for MEDLINE]
Free PMC Article

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