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NiCl2 (15 μM) stimulates the electroretinogram (ERG) b-wave amplitude of vertebrate retina up to 1.5-fold through its blocking of E/R-type voltage-gated Ca2+ channels. Assuming that such an increase is mediated by blocking the release of the inhibitory neurotransmitter γ-aminobutyric acid (GABA) via ionotropic GABA receptors, we tested the effect of both GABA itself and GABA-receptor antagonists such as (−)bicuculline (1.51-fold increase) and (1,2,5,6-tetrahydropyridin-4-yl)methylphosphinic acid (TPMPA; 1.46-fold increase) on the b-wave amplitude.Recording of the transretinal potentials from the isolated bovine retina.GABA (100 μM) reduced the b-wave amplitude only when NiCl2 (15 μM) was applied first. Each antagonist applied on its own stimulated the b-wave amplitude only partially: subsequent NiCl2 superfusion caused a small but additional increase, leading to a 1.69- and a 1.88-fold total increase of the amplitude by Ni2+ plus (−)bicuculline or Ni2+ plus TPMPA, respectively. Only the application of both antagonists in combination, before superfusing low NiCl2 (15 μM), completely prevented subsequent stimulation by NiCl2 with a similar 1.90-fold total increase of b-wave amplitude. Those retina segments that did not respond to NiCl2 could not be stimulated by (−)bicuculline and vice versa.The stimulatory effect of NiCl2 on the ERG b-wave amplitude is mainly, but not only, mediated by a NiCl2-sensitive, Cav2.3-triggered GABA release acting through ionotropic GABA-A and GABA-C receptors.