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.