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The Journal of Neuroscience, May 12, 2004, 24(19):4698-4708; doi:10.1523/JNEUROSCI.5523-03.2004

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 Previous Article

Cellular/Molecular
Ca2+-Binding Protein-1 Facilitates and Forms a Postsynaptic Complex with Cav1.2 (L-Type) Ca2+ Channels

Hong Zhou,1 * Seong-Ah Kim,1 * Elizabeth A. Kirk,1 Alyssa L. Tippens,1 Hong Sun,1 Françoise Haeseleer,2 and Amy Lee1

1Department of Pharmacology and Center for Neurodegenerative Disease, Emory University School of Medicine, Atlanta, Georgia 30322, and 2Department of Opthalmology, University of Washington School of Medicine, Seattle, Washington 98195

Ca2+-binding protein-1 (CaBP1) is a Ca2+-binding protein that is closely related to calmodulin (CaM) and localized in somatodendritic regions of principal neurons throughout the brain, but how CaBP1 participates in postsynaptic Ca2+ signaling is not known. Here, we describe a novel role for CaBP1 in the regulation of Ca2+ influx through Cav1.2 (L-type) Ca2+ channels. CaBP1 interacts directly with the {alpha}1 subunit of Cav1.2 at sites that also bind CaM. CaBP1 binding to one of these sites, the IQ domain, is Ca2+ dependent and competitive with CaM binding. The physiological significance of this interaction is supported by the association of Cav1.2 and CaBP1 in postsynaptic density fractions purified from rat brain. Moreover, in double-label immunofluorescence experiments, CaBP1 and Cav1.2 colocalize in numerous cell bodies and dendrites of neurons, particularly in pyramidal cells in the CA3 region of the hippocampus and in the dorsal cortex. In electrophysiological recordings of cells transfected with Cav1.2, CaBP1 greatly prolonged Ca2+ currents, prevented Ca2+-dependent inactivation, and caused Ca2+-dependent facilitation of currents evoked by step depolarizations and repetitive stimuli. These effects contrast with those of CaM, which promoted strong Ca2+-dependent inactivation of Cav1.2 with these same voltage protocols. Our findings reveal how Ca2+-binding proteins, such as CaM and CaBP1, differentially adjust Ca2+ influx through Cav1.2 channels, which may specify diverse modes of Ca2+ signaling in neurons.

Key words: calcium; calmodulin; channel; postsynaptic; facilitation; inactivation

Received Dec 16, 2003; revised April 12, 2004; accepted April 15, 2004.




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