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The Journal of Neuroscience, November 5, 2003, 23(31):10116-10121

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Cellular/Molecular
A Mechanism for the Direct Regulation of T-Type Calcium Channels by Ca2+/Calmodulin-Dependent Kinase II

Philip J. Welsby*,1 Hongge Wang*,1 Joshua T. Wolfe,1 Roger J. Colbran,2 Michael L. Johnson,1 and Paula Q. Barrett1

1Department of Pharmacology, University of Virginia, Charlottesville, Virginia 22908, and 2Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, Tennessee 37232

Low-voltage-activated (LVA) Ca2+ channels are widely distributed throughout the CNS and are important determinants of neuronal excitability, initiating dendritic and somatic Ca2+ spikes that trigger and shape the pattern of action potential firing. Here, we define a molecular mechanism underlying the dynamic regulation of {alpha}1H channels (Cav3.2), by Ca2+/CaM-dependent protein kinase II (CaMKII). We show that channel regulation is selective for the LVA {alpha}1H Ca2+ channel subtype, depends on determinants in the {alpha}1H II-III intracellular loop, and requires the phosphorylation of a serine residue absent from unregulated {alpha}1G (Cav3.1) channels. These studies identify the {alpha}1H channel as a new substrate for CaMKII and provide the first molecular mechanism for the direct regulation of T-type Ca2+ channels by a protein kinase. Our data suggest a novel mechanism for modulating the integrative properties of neurons.

Key words: calcium [Ca]; calmodulin; channel; dendrite; hippocampus; protein kinase; T-type

Received July 10, 2003; revised September 15, 2003; accepted September 15, 2003.




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