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Tetrodotoxin‐resistant voltage‐gated sodium channels Na v 1.8 and Na v 1.9 are expressed in the retina
Author(s) -
O'Brien Brendan J.,
Caldwell John H.,
Ehring George R.,
Bumsted O'Brien Keely M.,
Luo Songjiang,
Levinson S. Rock
Publication year - 2008
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.21701
Subject(s) - sodium channel , tetrodotoxin , retina , biology , neuroscience , nervous system , retinal ganglion cell , ganglion , biophysics , electrophysiology , microbiology and biotechnology , sodium , anatomy , chemistry , organic chemistry
Voltage‐gated sodium channels (VGSCs) are one of the fundamental building blocks of electrically excitable cells in the nervous system. These channels are responsible for the generation of action potentials that are required for the communication of neuronal signals over long distances within a cell. VGSCs are encoded by a family of nine genes whose products have widely varying biophysical properties. In this study, we have detected the expression of two atypical VGSCs (Na v 1.8 and Na v 1.9) in the retina. Compared with more common VGSCs, Na v 1.8 and Na v 1.9 have unusual biophysical and pharmacological properties, including persistent sodium currents and resistance to the canonical sodium channel blocker tetrodotoxin (TTX). Our molecular biological and immunohistochemical data derived from mouse ( Mus musculus ) retina demonstrate expression of Na v 1.8 by retinal amacrine and ganglion cells, whereas Na v 1.9 is expressed by photoreceptors and Müller glia. The fact that these channels exist in the central nervous system (CNS) and exhibit robust TTX resistance requires a re‐evaluation of prior physiological, pharmacological, and developmental data in the visual system, in which the diversity of VGSCs has been previously underestimated. J. Comp. Neurol. 508:940–951, 2008. © 2008 Wiley‐Liss, Inc.