Present address: Laboratory of Molecular and Cellular Neuroscience, The Rockefeller University, 1230 York Avenue, New York, NY 10021, USA.
An antibody to synaptotagmin I facilitates synaptic transmission
Article first published online: 6 JUN 2007
European Journal of Neuroscience
Volume 25, Issue 11, pages 3217–3225, June 2007
How to Cite
Hua, S.-Y., Teylan, M. A. and Cimenser, A. (2007), An antibody to synaptotagmin I facilitates synaptic transmission. European Journal of Neuroscience, 25: 3217–3225. doi: 10.1111/j.1460-9568.2007.05602.x
- Issue published online: 6 JUN 2007
- Article first published online: 6 JUN 2007
- Received 23 December 2006,revised 31 March 2007,accepted 20 April 2007
- EPSP rise time;
- neurotransmitter release;
- synaptic delay;
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+.