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Voltage-Dependent Calcium Channel Ca_V1.3 Subunits Regulate the Light Peak of the Electroretinogram

¹Cole Eye Institute, Cleveland Clinic Foundation, Cleveland, Ohio; ²Department of Ophthalmology and Vision Science, University of Arizona, Tucson, Arizona; ³Optical Sciences Center, University of Arizona, Tucson, Arizona; ⁴Abteilung Pharmakologie und Toxikologie, Institut fuer Pharmazie, Universitat Innsbruck, Innsbruck, Austria; ⁵Research Service, Cleveland Veterans Affairs Medical Center, Cleveland, Ohio; and ⁶Department of Ophthalmology, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, Ohio

Submitted 8 February 2007; accepted in final form 17 March 2007

In response to light, the mouse retinal pigment epithelium (RPE) generates a series of slow changes in potential that are referred to as the c-wave, fast oscillation (FO), and light peak (LP) of the electroretinogram (ERG). The LP is generated by a depolarization of the basolateral RPE plasma membrane by the activation of a calcium-sensitive chloride conductance. We have previously shown that the LP is reduced in both mice and rats by nimodipine, which blocks voltage-dependent calcium channels (VDCCs) and is abnormal in lethargic mice, carrying a null mutation in the calcium channel ₄ subunit. To define the ₁ subunit involved in this process, we examined mice lacking Ca_V1.3. In comparison with wild-type (WT) control littermates, LPs were reduced in Ca_V1.3^–/– mice. This pattern matched closely with that previously noted in lethargic mice, confirming a role for VDCCs in regulating the signaling pathway that culminates in LP generation. These abnormalities do not reflect a defect in rod photoreceptor activity, which provides the input to the RPE to generate the c-wave, FO, and LP, because ERG a-waves were comparable in WT and Ca_V1.3^–/– littermates. Our results identify Ca_V1.3 as the principal pore-forming subunit of VDCCs involved in stimulating the ERG LP.

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