HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 97/5/3731    most recent 00146.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Wu, J. Articles by Peachey, N. S. Search for Related Content PubMed PubMed Citation Articles by Wu, J. Articles by Peachey, N. S.

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.

This article has been cited by other articles:

				Y. Zhang, B. R. Davidson, W. D. Stamer, J. K. Barton, L. Y. Marmorstein, and A. D. Marmorstein Enhanced Inflow and Outflow Rates Despite Lower IOP in Bestrophin-2-Deficient Mice Invest. Ophthalmol. Vis. Sci., February 1, 2009; 50(2): 765 - 770. [Abstract] [Full Text] [PDF]

				M. A. McCall and R. G. Gregg Comparisons of structural and functional abnormalities in mouse b-wave mutants J. Physiol., September 15, 2008; 586(18): 4385 - 4392. [Abstract] [Full Text] [PDF]

				K. Yu, Q. Xiao, G. Cui, A. Lee, and H. C. Hartzell The Best Disease-Linked Cl- Channel hBest1 Regulates CaV1 (L-type) Ca2+ Channels via src-Homology-Binding Domains J. Neurosci., May 28, 2008; 28(22): 5660 - 5670. [Abstract] [Full Text] [PDF]

				B. Bakall, P. McLaughlin, J. B. Stanton, Y. Zhang, H. C. Hartzell, L. Y. Marmorstein, and A. D. Marmorstein Bestrophin-2 Is Involved in the Generation of Intraocular Pressure Invest. Ophthalmol. Vis. Sci., April 1, 2008; 49(4): 1563 - 1570. [Abstract] [Full Text] [PDF]