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Originally published In Press as doi:10.1074/jbc.M103724200 on August 20, 2001

J. Biol. Chem., Vol. 276, Issue 42, 38727-38737, October 19, 2001
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Functional Properties of CaV1.3 (alpha 1D) L-type Ca2+ Channel Splice Variants Expressed by Rat Brain and Neuroendocrine GH3 Cells*

Parsa SafaDagger §, Jim Boulter, and Tim G. HalesDagger ||

From the Dagger  Department of Pharmacology, The George Washington University, Washington, DC 20037, the § Neuroscience Interdepartmental Program, University of California, Los Angeles, California 90095, and the  Department of Psychiatry and Biobehavioral Sciences, Neuropsychiatric Institute, University of California, Los Angeles, California 90095

Ca2+ enters pituitary and pancreatic neuroendocrine cells through dihydropyridine-sensitive channels triggering hormone release. Inhibitory metabotropic receptors reduce Ca2+ entry through activation of pertussis toxin-sensitive G proteins leading to activation of K+ channels and voltage-sensitive inhibition of L-type channel activity. Despite the cloning and functional expression of several Ca2+ channels, those involved in regulating hormone release remain unknown. Using reverse transcription-polymerase chain reaction we identified mRNAs encoding three alpha 1 (alpha 1A, alpha 1C, and alpha 1D), four beta , and one alpha 2-delta subunit in rat pituitary GH3 cells; alpha 1B and alpha 1S transcripts were absent. GH3 cells express multiple alternatively spliced alpha 1D mRNAs. Many of the alpha 1D transcript variants encode "short" alpha 1D (alpha 1D-S) subunits, which have a QXXER amino acid sequence at their C termini, a motif found in all other alpha 1 subunits that couple to opioid receptors. The other splice variants identified terminate with a longer C terminus that lacks the QXXER motif (alpha 1D-L). We cloned and expressed the predominant alpha 1D-S transcript variants in rat brain and GH3 cells and their alpha lD-L counterpart in GH3 cells. Unlike alpha 1A channels, alpha 1D channels exhibited current-voltage relationships similar to those of native GH3 cell Ca2+ channels, but lacked voltage-dependent G protein coupling. Our data demonstrate that alternatively spliced alpha 1D transcripts form functional Ca2+ channels that exhibit voltage-dependent, G protein-independent facilitation. Furthermore, the QXXER motif, located on the C terminus of alpha 1D-S subunit, is not sufficient to confer sensitivity to inhibitory G proteins.

* The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

|| To whom correspondence should be addressed: Dept. of Pharmacology, Medical Center, The George Washington University, 2300 Eye St. NW, Washington, DC 20037. Tel.: 202-994-3546; Fax: 202-994-2870; E-mail: phmtgh@gwumc.edu.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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