Postsynaptic calcium pathway contributes to synaptic plasticity between retinal cones and luminosity-type horizontal cells.

It was previously found that the efficacy of synaptic transmission between retinal cone systems and luminosity-type horizontal cells (LHCs) was activity-dependent. Repetitive activation of red-cone pathway increased the LHCos hyperpolarizing response to red light, and the response enhancement was reversible. In this study, intracellular recording and pharmacological method were applied to investigate the mechanism(s) underlying red-flickering-induced response enhancement. Lowering intracellular Ca(2+) in the LHC by intracellular injection of Ca(2+) chelator EGTA prevented the development of red-flickering-induced response enhancement, which implicates the importance of postsynaptic calcium signal. The response enhancement could also be eliminated by a potent antagonist of Ca(2+)-permeable AMPA receptor (CP-AMPAR), which suggests the possibility that Ca(2+) influx via glutamate-gated calcium channels is related to the changes of [Ca(2+)](i). Furthermore, the administration of ryanodine or caffeine also attenuated the phenomenon, which gives evidence that the local calcium signal caused by intracellular calcium-induced calcium release (CICR) may be involved. Taken together, our data implicate that postsynaptic CICR and CP-AMPAR are related to the activity-dependent response enhancement.