Activation of Ca2+‐calmodulin kinase II induces desensitization by background light in dogfish retinal ‘on’ bipolar cells

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Abstract
1 Retinal ‘on’ bipolar cells possess a metabotropic glutamate receptor (mGluR6) linked to the control of a G‐protein and cGMP‐activated channels which functions to generate high synaptic amplification of rod signals under dark‐adapted conditions. 2 Desensitization of ‘on’ bipolar cells is initiated by a rise in Ca2+ during background light too weak to adapt rod photoreceptors. Desensitization could also be elicited by raising intracellular Ca2+ above 1 μm. 3 In order to investigate the mechanism of desensitization, whole‐cell current responses to brief flashes and to steps of light were obtained from voltage‐clamped ‘on’ bipolar cells in dark‐adapted dogfish retinal slices. The inclusion of Ca2+‐calmodulin kinase II (CaMKII) inhibitor peptides in the patch pipette solutions not only blocked desensitization of ‘on’ bipolar cells by dim background light and by 50 μm Ca2+, but also increased their flash sensitivity. 4 The substrate of phosphorylation by CaMKII is the ‘on’ bipolar cell cGMP‐activated channels. Desensitization probably results from a reduction in their sensitivity to cGMP and a voltage‐dependent decrease in their conductance. 5 A role for protein kinase C (PKC) in this process was excluded since activating PKC independently of Ca2+ with the phorbol ester PMA failed to induce desensitization of ‘on’ bipolar cells.