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Background  So far, only indirect evidence exists for the pharmacoresistant R-type voltage-gated Ca 2+  channel (VGCC) to be involved in transretinal signaling by triggering GABA-release onto ON-bipolar neurons. This release of inhibitory neurotransmitters was deduced from the sensitivity of the b-wave to stimulation by Ni 2+ , Zn 2+  and Cu 2+ . To further confirm the interpretation of these findings, we compared the effects of Cu 2+  application and chelation (using kainic acid, KA) on the neural retina from wildtype and Ca v 2.3-deficient mice. Furthermore, the immediately effect of KA on the ERG b-wave modulation was assessed.    Methods  Transretinal signaling was recorded as an ERG from the superfused murine retina isolated from wildtype and Ca v 2.3-deficient mice.    Results  In mice, the stimulating effect of 100 nM CuCl 2  is absent in the retinae from Ca v 2.3-deficient mice, but prominent in Ca v 2.3-competent mice. Application of up to 3 mM tricine does not affect the murine b-wave in both genotypes, most likely because of chelating amino acids present in the murine nutrient solution. Application of 27 μM KA significantly increased the b-wave amplitude in wild type and Ca v 2.3 (−|-) mice. This effect can most likely be explained by the stimulation of endogenous KA-receptors described in horizontal, OFF-bipolar, amacrine or ganglion cells, which could not be fully blocked in the present study.    Conclusion  Cu 2+ -dependent modulation of transretinal signaling only occurs in the murine retina from Ca v 2.3 competent mice, supporting the ideas derived from previous work in the bovine retina that R-type Ca 2+  channels are involved in shaping transretinal responses during light perception.

Submicromolar copper (II) ions stimulate transretinal signaling in the isolated retina from wild type but not from Cav2.3-deficient mice