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This Article Full Text Full Text (PDF) All Versions of this Article: 101/1/42    most recent 91103.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Gu, H. Articles by O'Dowd, D. K. Search for Related Content PubMed PubMed Citation Articles by Gu, H. Articles by O'Dowd, D. K.

Ca_v2-Type Calcium Channels Encoded by cac Regulate AP-Independent Neurotransmitter Release at Cholinergic Synapses in Adult Drosophila Brain

Departments of Anatomy and Neurobiology; Developmental and Cell Biology, University of California, Irvine, California

Submitted 2 October 2008; accepted in final form 7 November 2008

Voltage-gated calcium channels containing 1 subunits encoded by Ca_v2 family genes are critical in regulating release of neurotransmitter at chemical synapses. In Drosophila, cac is the only Ca_v2-type gene. Cacophony (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 neuromuscular junction (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 (PNs) examined in adult brains, express calcium currents with two components: a slow-inactivating current sensitive to the spider toxin Plectreurys toxin II (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 mutant neurons both in culture and in whole brain recordings is a reduced cholinergic miniature excitatory postsynaptic current frequency that is mimicked in wild-type neurons by acute application of PLTXII. These data demonstrate that cac encoded Ca_v2-type calcium channels regulate action potential (AP)-independent release of neurotransmitter at excitatory cholinergic synapses in the adult brain, a function not predicted from studies at the larval NMJ.