Submitted on October 2, 2008
Revised on November 6, 2008
Accepted on November 7, 2008
Cav2-type calcium channels encoded by cac regulate AP-independent neurotransmitter release at cholinergic synapses in adult Drosophila brain
Huaiyu Gu1, Shaojuan Amy Jiang1, Jorge M. Campusano2, Jorge Iniguez1, Hailing Su, Andy A Hoang1, Monica Lavian1, Xicui Sun3, and Diane K O'Dowd4*
1 University of California Irvine
2 University of California, Irvine
3 University of California Irv
4 Univeristy of California - Irvine
* To whom correspondence should be addressed. E-mail: dkodowd{at}uci.edu.
Voltage-gated calcium channels containing 
1 subunits encoded by Cav2 family genes are critical in regulating release of neurotransmitter at chemical synapses. In Drosophila, cac is the only Cav2-type gene. CAC channels are localized in motor neuron terminals where they have been shown to mediate evoked, but not AP-independent, release of glutamate at the larval NMJ. Cultured embryonic neurons also express CAC channels but there is no information about the properties of CAC-mediated currents in adult brain, nor how these channels regulate transmission in central neural circuits where fast excitatory synaptic transmission is predominantly cholinergic. Here we report that wild-type neurons cultured from late stage pupal brains and antennal lobe projection neurons (PN) examined in adult brains, express calcium currents with two components: a slow-inactivating current sensitive to the spider toxin PLTXII and a fast-inactivating PLTXII-resistant component. CAC channels are the major contributors to the slow-inactivating PLTXII-sensitive current based on selective reduction of this component in hypomorphic cac mutants (NT27 and TS3). Another characteristic of cac neurons both in culture and in whole brain recordings is a reduced cholinergic mEPSC frequency that is mimicked in wild-type neurons by acute application of PLTXII. These data demonstrate that cac encoded Cav2-type calcium channels regulate AP-independent release of neurotransmitter at excitatory cholinergic synapses in the adult brain, a function not predicted from studies at the larval NMJ.
