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• W2010178856 abstract "To resolve some of differences in reports on the function of Synaptotagmin I (Syt I), we re-examined synaptic transmission at the neuromuscular junction of Drosophila embryos that have mutations in the Syt I gene ( syt I). Two major questions addressed were which Ca 2+ binding domain, C2A or C2B, sense Ca 2+ and is Syt I a negative regulator of spontaneous vesicle fusion. Synaptic currents were induced by nerve stimulation or by high K + treatment in external solutions containing various Ca 2+ concentrations. In a null allele, syt I AD4 , synchronous synaptic currents were rarely observed but not abolished. The quantal content was about 1/60 of control but increased linearly with [Ca 2+ ] e with a slope of 0.95 ( N) in the double logarithmic plot, in contrast to 3.01 in control. The slope of 1.06 in an allele, syt I AD1 , which lacks the second Ca 2+ binding domain, C2B, was not different from in syt I AD4 . In another allele, syt I AD3 , in which one amino acid in C2B is mutated, synchronous synaptic transmission was also impaired and N was 1.54, which is significantly smaller than in control. In high K + saline, the [Ca 2+ ] e dependency of vesicle release in syt I AD4 was lower than in controls, whereas that in syt I AD3 was even lower than in syt I AD4 , suggesting that syt I AD3 is inhibiting vesicle fusion. These findings led us to conclude that C2B, not C2A, senses Ca 2+ , and Syt I is a negative regulator of vesicle fusion." @default.
• W2010178856 created "2016-06-24" @default.
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• W2010178856 date "2005-08-01" @default.
• W2010178856 modified "2023-09-30" @default.
• W2010178856 title "External Ca²⁺Dependency of Synaptic Transmission in<i>Drosophila synaptotagmin I</i>Mutants" @default.
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• W2010178856 doi "https://doi.org/10.1152/jn.00205.2005" @default.
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