Delayed Synaptic Transmission in Drosophila cacophony Embryos

Hou J, Tamura T, Kidokoro Y. Delayed symaptic transmission in Drosophila cacophony embryos. J Neurophysiol 100: 2833–2842, 2008. First published September 24, 2008; doi:10.1152/jn.90342.2008. Ca influx through the Drosophila N-type Ca channel, encoded by cacophony (cac), triggers fast synaptic transmission. We now ask whether the cac Ca channel is the Ca channel solely dedicated for fast synaptic transmission. Because the cac mutation is lethal, we used cac 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 background, fast synaptic transmission recovered. However, even in cac embryos, nerve stimulation infrequently induced delayed synaptic events in the minority of cells in 1.5 mM [Ca ]e and in the majority of cells in 5 mM [Ca 2 ]e. The number of delayed quantal events per stimulus was greater in 5 mM [Ca ]e than in 1.5 mM. Thus the delayed release is [Ca ]e dependent. Plectreurys toxin II (PLTXII) (10 nM; a spider toxin analog) depressed the frequency of delayed events, suggesting that voltage-gated Ca channels, other than cac Ca channels, are contributing to them. However, delayed events were not affected by 50 M La . The frequency of miniature synaptic currents in cac 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 embryos. Taken together, the cac Ca channel is indispensable for fast synaptic transmission in normal conditions, and another type of Ca channel, the non-cac, PLTXII-sensitive Ca channel, is contributing to delayed release in cac embryos.