title: Delayed synaptic transmission in Drosophila cacophonynull embryos.
abstract: Ca(2+) influx through the Drosophila N-type Ca(2+) channel, encoded by cacophony (cac), triggers fast synaptic transmission. We now ask whether the cac Ca(2+) channel is the Ca(2+) 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 [Ca(2+)](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(2+)](e) than in 1.5 mM. Thus the delayed release is [Ca(2+)](e) dependent. Plectreurys toxin II (PLTXII) (10 nM; a spider toxin analog) depressed the frequency of delayed events, suggesting that voltage-gated Ca(2+) channels, other than cac Ca(2+) channels, are contributing to them. However, delayed events were not affected by 50 microM La(3+). The frequency of miniature synaptic currents in cac(null) embryos was approximately 1/2 of control, whereas in high K(+) solutions, it was approximately 1/135. The hypertonicity response was approximately 1/10 of control. These findings indicate that the number of release-ready vesicles is smaller in cac(null) embryos. Taken together, the cac Ca(2+) channel is indispensable for fast synaptic transmission in normal conditions, and another type of Ca(2+) channel, the non-cac, PLTXII-sensitive Ca(2+) channel, is contributing to delayed release in cac(null) embryos.
authors.affiliation: Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Japan.
authors.forename: Jiamei
authors.initials: J
authors.lastname: Hou
authors.forename: Takuya
authors.initials: T
authors.lastname: Tamura
authors.forename: Yoshiaki
authors.initials: Y
authors.lastname: Kidokoro
mesh_terms: D000009:Abdominal Muscles / Q000196:embryology / Q000502:physiology / Q000528:radiation effects; D000704:Analysis of Variance; D000818:Animals; D030801:Animals, Genetically Modified; D002118:Calcium / Q000378:metabolism; D015220:Calcium Channels / Q000172:deficiency*; D004330:Drosophila; D029721:Drosophila Proteins / Q000172:deficiency* / Q000235:genetics; D004558:Electric Stimulation; D004625:Embryo, Nonmammalian; D049452:Green Fluorescent Proteins / Q000096:biosynthesis / Q000378:metabolism; D006982:Hypertonic Solutions / Q000494:pharmacology; D009154:Mutation; D009469:Neuromuscular Junction / Q000187:drug effects / Q000502:physiology*; D018408:Patch-Clamp Techniques / Q000379:methods; D011930:Reaction Time / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects; D013111:Spider Venoms / Q000494:pharmacology; D009435:Synaptic Transmission / Q000187:drug effects / Q000235:genetics*; D013696:Temperature; D013997:Time Factors
chemical_list: D015220:Calcium Channels; D029721:Drosophila Proteins; D006982:Hypertonic Solutions; C083634:PLTX-II; D013111:Spider Venoms; C472405:cac protein, Drosophila; D049452:Green Fluorescent Proteins; D002118:Calcium