RT Journal Article
SR Electronic
T1 <em>Drosophila cacophony</em> Channels: A Major Mediator of Neuronal Ca<sup>2+</sup> Currents and a Trigger for K<sup>+</sup> Channel Homeostatic Regulation
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 1072
OP 1081
DO 10.1523/JNEUROSCI.4746-06.2007
VO 27
IS 5
A1 I-Feng Peng
A1 Chun-Fang Wu
YR 2007
UL http://www.jneurosci.org/content/27/5/1072.abstract
AB The cacophony (cac) locus in Drosophila encodes a Ca2+ channel α subunit, but little is known about properties of cac-mediated currents and functional consequences of cac mutations in central neurons. We found that, in Drosophila cultured neurons, Ca2+ currents were mediated predominantly by the cac channels. The cac channels contribute to low- and high-threshold, fast- and slow-inactivating types of Ca2+ currents, take part in membrane depolarization, and strongly activate Ca2+-activated K+ current [I K(Ca)]. In cac neurons, unexpectedly, voltage-activated transient K+ current I A is upregulated to a level that matches I K(Ca) reduction, implicating a homeostatic regulation that was mimicked by chronic pharmacological blockade of Ca2+ currents in wild-type neurons. Among K+ channel transcripts, Shaker mRNA levels were preferentially increased in cac flies. However, Ca2+ current expression levels remained unaltered in several K+ channel mutants, illustrating a key role of cac in developmental regulation of Drosophila neuronal excitability.