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Delayed Synaptic Transmission in Drosophila cacophony^null Embryos

Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Japan

Submitted 7 March 2008; accepted in final form 18 September 2008

Ca²⁺ influx through the Drosophila N-type Ca²⁺ channel, encoded by cacophony (cac), triggers fast synaptic transmission. We now ask whether the cac Ca²⁺ channel is the Ca²⁺ channel solely dedicated for fast synaptic transmission. Because the cac^null mutation is lethal, we used cac^null embryos to address this question. At the neuromuscular junction in HL3 solution, no fast synchronous synaptic transmission was detected on nerve stimulation. When the wild-type cac gene was introduced in the cac^null background, fast synaptic transmission recovered. However, even in cac^null embryos, nerve stimulation infrequently induced delayed synaptic events in the minority of cells in 1.5 mM [Ca²⁺]_e and in the majority of cells in 5 mM [Ca²⁺]_e. The number of delayed quantal events per stimulus was greater in 5 mM [Ca²⁺]_e than in 1.5 mM. Thus the delayed release is [Ca²⁺]_e dependent. Plectreurys toxin II (PLTXII) (10 nM; a spider toxin analog) depressed the frequency of delayed events, suggesting that voltage-gated Ca²⁺ channels, other than cac Ca²⁺ channels, are contributing to them. However, delayed events were not affected by 50 µM La³⁺. The frequency of miniature synaptic currents in cac^null embryos was 1/2 of control, whereas in high K⁺ solutions, it was 1/135. The hypertonicity response was 1/10 of control. These findings indicate that the number of release-ready vesicles is smaller in cac^null embryos. Taken together, the cac Ca²⁺ channel is indispensable for fast synaptic transmission in normal conditions, and another type of Ca²⁺ channel, the non-cac, PLTXII-sensitive Ca²⁺ channel, is contributing to delayed release in cac^null embryos.

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