PT - JOURNAL ARTICLE AU - Kawasaki, Fumiko AU - Felling, Ryan AU - Ordway, Richard W. TI - A Temperature-Sensitive Paralytic Mutant Defines a Primary Synaptic Calcium Channel in <em>Drosophila</em> AID - 10.1523/JNEUROSCI.20-13-04885.2000 DP - 2000 Jul 01 TA - The Journal of Neuroscience PG - 4885--4889 VI - 20 IP - 13 4099 - http://www.jneurosci.org/content/20/13/4885.short 4100 - http://www.jneurosci.org/content/20/13/4885.full SO - J. Neurosci.2000 Jul 01; 20 AB - Neurotransmission at chemical synapses involves regulated exocytosis of neurotransmitter from the presynaptic terminal. Neurotransmitter release is thought to be triggered by calcium influx through specific classes of voltage-gated calcium channels. Here we report genetic and functional analysis implicating a specific calcium channel gene product in neurotransmitter release. We have isolated a temperature-sensitive paralytic allele of the Drosophilacalcium channel α1 subunit gene, cacophony(cac). This mutant, referred to ascacTS2, allows functional analysis of synaptic transmission after acute perturbation of a specific α1 subunit. Electrophysiological analysis at neuromuscular synapses revealed that neurotransmitter release incacTS2 is markedly reduced at elevated temperatures, indicating that cac encodes a primary α1 subunit functioning in synaptic transmission. These observations further define the molecular basis of voltage-gated calcium entry at synapses and provide a new starting point for further genetic analysis of synaptic mechanisms.