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C. Joselevitch, M. Kamermans; Dendritic Potassium Channels in Mixed–Input on Bipolar Cells . Invest. Ophthalmol. Vis. Sci. 2005;46(13):1123.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: : Rod–driven light responses in mixed–input ON BCs (ON MBCs) of the goldfish are a conductance increase mediated by a metabotropic glutamate receptor (mGluR). Activation of this mGluR with AP–4 induces a linear conductance decrease with a reversal potential near 0 mV (Nawy and Copenhagen, 1987; Thoreson and Miller, 1993). Puffs of AP–4 in the goldfish OPL also induce a linear conductance decrease with a reversal potential near 0 mV in ON MBCs, but their rod–driven light responses rectify at positive potentials and do not reverse at 0 mV. The cone–driven light responses of these BCs (which are a conductance decrease with a negative reversal potential) also rectify at positive potentials, indicating that the rectification is a post–synaptic process. Methods: Whole–cell patch–clamp recordings from ON MBCs were obtained in retinal slices. After anatomic reconstruction of a lucifer yellow–filled cell, a model was formulated using the NEURON simulation environment to account for ON MBC response properties. Results: The rectification of light–driven conductances in ON MBCs coincides with the activation of an outwardly rectifying K+–current; bath application of 4–AP reduced this rectification. Model simulations indicate that while somatic K+–currents do not influence light–driven responses, dendritic K+–channels shift reversal potentials and increase the rectification considerably. Due to the high resistance of the ON MBC dendrites in the rod terminal, synaptic inputs and AP–4 puffs can yield different results. Conclusions: Dendritic K+–channels speed up synaptic transmission and generate transience at the first synapse by accelerating the repolarization of ON MBCs. Additionally, if the glutamate release of the rods is continuously suppressed, the combination of glutamate–gated and voltage–gated conductances brings the cell to a more depolarized resting membrane potential, increasing the driving force for cone–driven light responses. The converse is also true: in the dark, the continuous glutamate release of the cones enhances rod–driven light responses by keeping ON MBCs hyperpolarized.
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