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1 Ophthalmic Research, Cleveland Clinic Foundation, Cleveland, Ohio, United States
2 Ophthalmology and Visual Science, University of Arizona, Tucson, Arizona, United States
3 Institut fuer Pharmazie, Universitat Innsbruck, Innsbruck, Austria
4 Ophthalmic Research, Cleveland Clinic Foundation, cleveland, Ohio, United States
* To whom correspondence should be addressed. E-mail: neal.peachey{at}va.gov.
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 CaV1.3. In comparison to wild-type control littermates, LPs were reduced in CaV1.3-/- 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, since ERG a-waves were comparable in WT and CaV1.3-/- littermates. Our results identify CaV1.3 as the principal pore-forming subunit of VDCCs involved in stimulating the ERG LP.
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