Visual Neuroscience

Research Articles

Expression and modulation of connexin30.2, a novel gap junction protein in the mouse retina

LUIS PÉREZ DE SEVILLA MÜLLERa1 p1, KARIN DEDEKa1, ULRIKE JANSSEN-BIENHOLDa1, ARNDT MEYERa1, MARIA M. KREUZBERGa2, SUSANNE LORENZa1, KLAUS WILLECKEa2 and RETO WEILERa1 c1

a1 Department of Neurobiology, University of Oldenburg, Oldenburg, Germany

a2 Institute for Genetics, University of Bonn, Bonn, Germany

Abstract

Mammalian retinae express multiple connexins that mediate the metabolic and electrical coupling of various cell types. In retinal neurons, only connexin36, connexin45, connexin50, and connexin57 have been described so far. Here, we present an analysis of a novel retinal connexin, connexin30.2 (Cx30.2), and its regulation in the mouse retina. To analyze the expression of Cx30.2, we used a transgenic mouse line in which the coding region of Cx30.2 was replaced by lacZ reporter DNA. We detected the lacZ signal in the nuclei of neurons located in the inner nuclear layer and the ganglion cell layer (GCL). In this study, we focused on the GCL and characterized the morphology of the Cx30.2-expressing cells. Using immunocytochemistry and intracellular dye injections, we found six different types of Cx30.2-expressing ganglion cells: one type of ON-OFF, three types of OFF, and two types of ON ganglion cells; among the latter was the RGA1 type. We show that RGA1 cells were heterologously coupled to numerous displaced amacrine cells. Our results suggest that these gap junction channels may be heterotypic, involving Cx30.2 and a connexin yet unidentified in the mouse retina. Gap junction coupling can be modulated by protein kinases, a process that plays a major role in retinal adaptation. Therefore, we studied the protein kinase–induced modulation of coupling between RGA1 and displaced amacrine cells. Our data provide evidence that coupling of RGA1 cells to displaced amacrine cells is mediated by Cx30.2 and that the extent of this coupling is modulated by protein kinase C.

(Received September 14 2009)

(Accepted April 14 2010)

(Online publication June 11 2010)

Correspondence:

c1 Address correspondence and reprint requests to: Professor Reto Weiler, Department of Neurobiology, University of Oldenburg, P.O. Box 2503, D-26111 Oldenburg, Germany. E-mail: reto.weiler@uni-oldenburg.de

p1 Present address: Retina and Optic Nerve Research Laboratory, Department of Anatomy & Neurobiology, Dalhousie University, Halifax, Nova Scotia, Canada.