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The Journal of Neuroscience, January 31, 2007, 27(5):1072-1081; doi:10.1523/JNEUROSCI.4746-06.2007

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Development/Plasticity/Repair
Drosophila cacophony Channels: A Major Mediator of Neuronal Ca²⁺ Currents and a Trigger for K⁺ Channel Homeostatic Regulation

I-Feng Peng and Chun-Fang Wu

Department of Biological Sciences, University of Iowa, Iowa City, Iowa 52242

Correspondence should be addressed to Chun-Fang Wu, Department of Biological Sciences, University of Iowa, Iowa City, IA 52242. Email: chun-fang-wu{at}uiowa.edu

The cacophony (cac) locus in Drosophila encodes a Ca²⁺ channel 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.

Key words: cac; Dmca1A; ion channel regulation; real-time PCR; compensatory regulation; Ca channel mutations

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Received Oct. 31, 2006; revised Dec. 20, 2006; accepted Dec. 21, 2006.

Correspondence should be addressed to Chun-Fang Wu, Department of Biological Sciences, University of Iowa, Iowa City, IA 52242. Email: chun-fang-wu{at}uiowa.edu

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