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The Journal of Neuroscience, May 13, 2009, 29(19):6088-6093; doi:10.1523/JNEUROSCI.0132-09.2009

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Brief Communications
A Transient Receptor Potential-Like Channel Mediates Synaptic Transmission in Rod Bipolar Cells

Yin Shen,^1,2 J. Alexander Heimel,³ Maarten Kamermans,^4,5 Neal S. Peachey,^6,7,8 Ronald G. Gregg,^9,10 and Scott Nawy^1,2

¹Departments of Ophthalmology and Visual Sciences and ²Dominick P. Purpura Department of Neuroscience, Albert Einstein College of Medicine, Bronx, New York 10461, ³Molecular Visual Plasticity Group and ⁴Research Unit Retinal Signal Processing, The Netherlands Institute for Neuroscience, Royal Netherlands Academy of Arts and Sciences, 1105 BA Amsterdam, The Netherlands, ⁵Department of Neurogenetics, Academic Medical Center, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands, ⁶Cleveland Veterans Affairs Medical Center, Cleveland, Ohio 44196, ⁷Cole Eye Institute, Cleveland Clinic Foundation, Cleveland, Ohio 44195, ⁸Department of Ophthalmology, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, Ohio 44106, and Departments of ⁹Biochemistry and Molecular Biology and ¹⁰Ophthalmology and Visual Sciences, University of Louisville, Louisville, Kentucky 40202

Correspondence should be addressed to Yin Shen, Dominick P. Purpura Department of Neuroscience, Albert Einstein College of Medicine, Bronx, NY 10461. Email: yshen{at}aecom.yu.edu

On bipolar cells are connected to photoreceptors via a sign-inverting synapse. At this synapse, glutamate binds to a metabotropic receptor which couples to the closure of a cation-selective transduction channel. The molecular identity of both the receptor and the G protein are known, but the identity of the transduction channel has remained elusive. Here, we show that the transduction channel in mouse rod bipolar cells, a subtype of On bipolar cell, is likely to be a member of the TRP family of channels. To evoke a transduction current, the metabotropic receptor antagonist LY341495 was applied to the dendrites of cells that were bathed in a solution containing the mGluR6 agonists L-AP4 or glutamate. The transduction current was suppressed by ruthenium red and the TRPV1 antagonists capsazepine and SB-366791. Furthermore, focal application of the TRPV1 agonists capsaicin and anandamide evoked a transduction-like current. The capsaicin-evoked and endogenous transduction current displayed prominent outward rectification, a property of the TRPV1 channel. To test the possibility that the transduction channel is TRPV1, we measured rod bipolar cell function in the TRPV1^–/– mouse. The ERG b-wave, a measure of On bipolar cell function, as well as the transduction current and the response to TRPV1 agonists were normal, arguing against a role for TRPV1. However, ERG measurements from mice lacking TRPM1 receptors, another TRP channel implicated in retinal function, revealed the absence of a b-wave. Our results suggest that a TRP-like channel, possibly TRPM1, is essential for synaptic function in On bipolar cells.

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Received Jan. 10, 2009; revised March 12, 2009; accepted March 15, 2009.

Correspondence should be addressed to Yin Shen, Dominick P. Purpura Department of Neuroscience, Albert Einstein College of Medicine, Bronx, NY 10461. Email: yshen{at}aecom.yu.edu

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