Intracellular calcium reduces light-induced excitatory post-synaptic responses in salamander retinal ganglion cells

1. The whole-cell patch clamp technique was used to study the effect of intracellular Ca2+ on light evoked EPSCs: in on-off ganglion cells in salamander retinal slices. Both AR IPA and NMDA receptors contributed to the light-evoked responses. 2. In the presence of strychnine and picrotoxin, ganglion cells responded to light onset and offset with transient inward currents at -70 mV. These currents were reduced by 35 +/- 3 % when the light stimulus was preceded hy a depolarizing step from -70 to 0 mV. 3. The inhibitory effect of depolarization on light-evoked EPSCs was strongly reduced in the presence of 10 mM BAPTA. 4. The degree of EPSC inhibition by the prepulse holding potential followed the current-voltage relationship of the Ca2+ current found in the ganglion cell., 5. In the presence of the NMDA receptor antagonist AP-7, glutamate-dependent current was nearly abolished when high Ca2+ was substituted for high Na+ solution. 6. The release of Ca2+ from internal stores by caffeine or inositol trisphosphate reduced the EPSCs by 36 +/- 5 and 38 +/- 11 %, respectively, and abolished the inhibitory effect of depolarization. 7. The inhibitory effect of depolarization on EPSCs was reduced 5-fold in the presence of AP-7, but with not reduced by the AMPA receptor antagonist CNQX. 8. Neither inhibition of Ca2+-calmodulin-dependent enzymes, nor inhibition of protein kinase A or C had any significant effect on the depolarization-induced inhibition of EPSCs. 9. Our data suggest that elevation of [Ca2+](i), through voltage-gated channels or by release from intracellular stores, reduced primarily the NMDA component of the light-evoked EPSCs.