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The Journal of Neuroscience, July 16, 2003, 23(15):6238-6244

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Differential Regulation of Transmitter Release by Alternatively Spliced Forms of Synaptotagmin I

Arash Nakhost,^1 * Gry Houeland,^2 * Vincent F. Castellucci,² and Wayne S. Sossin¹

¹Department of Neurology and Neurosurgery, McGill University, Montreal Neurological Institute, Montreal, Quebec, Canada H3A 2B4, and ²Department of Physiology, University of Montreal, Montreal, Quebec, Canada H3C 3J7

We discovered a novel alternatively spliced form of synaptotagmin I (Syt I). This splicing event is conserved over evolution and, in Aplysia, results in a two amino acid insert in the juxtamembrane domain of Syt I (Syt I_VQ). Both Syt I and Syt I_VQ are localized to synaptic vesicles; however, we also observed punctae that contained one or the other spliced products. Both Syt I and Syt I_VQ are phosphorylated at the adjacent PKC site. Overexpression of Syt I_VQ, but not of Syt I, in Aplysia neurons blocked the ability of serotonin to reverse synaptic depression. This effect is upstream of PKC activation, because neither Syt I_VQ nor Syt I blocked the effects of phorbol esters on reversing synaptic depression or the effects of serotonin on facilitating nondepressed synapses. Our results demonstrate a physiological role for splicing in the juxtamembrane domain of Syt I.

Key words: synaptotagmin; transmitter release; protein kinase C; PKC; Aplysia; depressed synapses; alternative splicing

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Received Oct. 17, 2002; revised May. 13, 2003; accepted May. 21, 2003.

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