Delayed Synaptic Transmission in Drosophila cacophonynull Embryos

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Abstract
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 cacnull embryos.