An antibody to synaptotagmin I facilitates synaptic transmission

Authors

  • Shao-Ying Hua,

    1. Department of Biological Sciences, Barnard College, Columbia University, 3009 Broadway, New York, NY, 10027, USA
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  • Merilee A. Teylan,

    1. Department of Biological Sciences, Barnard College, Columbia University, 3009 Broadway, New York, NY, 10027, USA
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    • *

      Present address: Laboratory of Molecular and Cellular Neuroscience, The Rockefeller University, 1230 York Avenue, New York, NY 10021, USA.

  • Aylin Cimenser

    1. Center for Theoretical Neuroscience, Center for Neurobiology and Behavior, Kolb Research Annex, Columbia University, 1051 Riverside Drive, New York, NY 10032-2695, USA
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Dr S.-Y. Hua, as above.
E-mail: shua@barnard.edu

Abstract

Proper functioning of the nervous system requires precise control of neurotransmitter release. Synaptotagmin, a synaptic vesicle protein, is crucial for the temporal control of neurotransmitter release. The mechanism of synaptotagmin function is still under debate. To investigate the mechanism by which synaptotagmin controls neurotransmitter release, we injected an antibody of rat synaptotagmin I into a crayfish motor axon. We found that the antibody enhanced synaptic transmission at crayfish neuromuscular junctions by increasing the amplitude of the evoked synaptic response. This effect was antibody-dose dependent. The antibody also reduced the rise time of the synaptic potentials. These effects were accompanied by a reduction in the Hill coefficient for Ca2+-dependence of synaptic transmission. Our findings support the hypothesis that synaptotagmin inhibits neurotransmitter release in the absence of Ca2+.

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