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J Neurophysiol 100: 868-878, 2008. First published June 11, 2008; doi:10.1152/jn.90464.2008
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Characterization of Voltage-Dependent Ca2+ Currents in Identified Drosophila Motoneurons In Situ

Jason W. Worrell1,2 and Richard B. Levine1,2,3

1Division of Neurobiology, 2Graduate Program in Physiological Sciences, and 3Department of Physiology, University of Arizona, Tucson, Arizona

Submitted 13 April 2008; accepted in final form 5 June 2008

Voltage-dependent Ca2+ channels contribute to neurotransmitter release, integration of synaptic information, and gene regulation within neurons. Thus understanding where diverse Ca2+ channels are expressed is an important step toward understanding neuronal function within a network. Drosophila provides a useful model for exploring the function of voltage-dependent Ca2+ channels in an intact system, but Ca2+ currents within the central processes of Drosophila neurons in situ have not been well described. The aim of this study was to characterize voltage-dependent Ca2+ currents in situ from identified larval motoneurons. Whole cell recordings from the somata of identified motoneurons revealed a significant influence of extracellular Ca2+ on spike shape and firing rate. Using whole cell voltage clamp, along with blockers of Na+ and K+ channels, a Ca2+-dependent inward current was isolated. The Drosophila genome contains three genes with homology to vertebrate voltage-dependent Ca2+ channels: Dmca1A, Dmca1D, and Dm{alpha}1G. We used mutants of Dmca1A and Dmca1D as well as targeted expression of an RNAi transgene to Dmca1D to determine the genes responsible for the voltage-dependent Ca2+ current recorded from two identified motoneurons. Our results implicate Dmca1D as the major contributor to the voltage-dependent Ca2+ current recorded from the somatodendritic processes of motoneurons, whereas Dmca1A has previously been localized to the presynaptic terminal where it is essential for neurotransmitter release. Altered firing properties in cells from both Dmca1D and Dmca1A mutants indicate a role for both genes in shaping firing properties.


Address for reprint requests and other correspondence: R. Levine, Division of Neurobiology, University of Arizona, Tucson, AZ 85721 (E-mail: RBL{at}neurobio.arizona.edu)




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H. Gu, S. A. Jiang, J. M. Campusano, J. Iniguez, H. Su, A. A. Hoang, M. Lavian, X. Sun, and D. K. O'Dowd
Cav2-Type Calcium Channels Encoded by cac Regulate AP-Independent Neurotransmitter Release at Cholinergic Synapses in Adult Drosophila Brain
J Neurophysiol, January 1, 2009; 101(1): 42 - 53.
[Abstract] [Full Text] [PDF]




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