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Proceedings of the National Academy of Sciences of the United States of America logoLink to Proceedings of the National Academy of Sciences of the United States of America
. 1995 Nov 21;92(24):11307–11311. doi: 10.1073/pnas.92.24.11307

Evidence for synaptotagmin as an inhibitory clamp on synaptic vesicle release in Aplysia neurons.

K C Martin 1, Y Hu 1, B A Armitage 1, S A Siegelbaum 1, E R Kandel 1, B K Kaang 1
PMCID: PMC40621  PMID: 7479985

Abstract

While previous studies have demonstrated that synaptotagmin plays an essential role in evoked neurotransmitter release, it has been difficult to determine whether it acts to facilitate or inhibit release. To address this question, we used acute genetic manipulations to alter the expression of synaptotagmin in Aplysia neurons. Transient overexpression of synaptotagmin in acutely dissected cholinergic neurons and in cultured glutaminergic neurons decreased the amplitude of the excitatory postsynaptic potential (EPSP) by 32% and 26%, respectively. In contrast, treatment of cultured presynaptic neurons with synaptotagmin antisense oligonucleotides increased the amplitude of the EPSP by 50-75%. These results are consistent with a role of synaptotagmin as an inhibitor of release.

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Selected References

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