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

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Abstract
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 AMPA 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 by 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 was 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.