Abstract
Abstract: :
Purpose: Changes in excitatory postsynaptic current (EPSC) kinetics as a result of changes in N-methyl-D-aspartate receptor (NMDAR) properties are reported to regulate periods of plasticity in different cortical areas including the visual cortex. In order to learn whether similar changes also occur in the retina, spontaneous and electrically evoked EPSCs were investigated in rat retinal ganglion cells (RGCs) during postnatal retinal development. Methods: Whole cell recordings of EPSCs in the voltage-clamp mode were performed on identified RGCs in a slice preparation of the pigmented rat retina. Electrical stimulation (50 µs - 50 ms, 5 - 400 mA) was applied by bipolar AgCl electrodes placed in the IPL. The NMDAR-mediated EPSC component (NMDAR-EPSC) was isolated by application of the non-NMDAR antagonist CNQX. Results: Before eye opening, electrical stimulation resulted in large, long-duration EPSCs with a mean amplitude of –249 pA (+ 156 pA, SD) and a time to peak value of 565 ms (+316 ms). At postnatal day 30 (P30), EPSC amplitude decreased to a mean value of 99 pA (+ 61 pA) and EPSC kinetics became significantly faster (Time to peak: 102 ms (+50 ms)). NMDAR-EPSC kinetics also showed age-dependent changes, with faster kinetics at older developmental stages. Time to peak values decreased from 875.5 ms (± 513.0 ms) at P9-12 to 230.1 ms (± 244.3 ms) at P30. In parallel, EPSC inactivation rates (τinact) decreased from 1727.8 ms (± 810,6 ms) to 259.4 ms (±196.2 ms) at P30. As for the evoked EPSCs, the time course of spontaneous EPSCs showed similar age-dependent changes. Conclusions: Our data clearly indicate a developmental fastening of NMDA-EPSC kinetics in rat RGCs comparable to what has been observed in higher brain areas. Togehter with our previous finding of a light-dependent decrease in NMDAR current amplitudes (Albach et al., Invest. phthalmol. Vis. Sci. 43, Supplement, 2707, 2002), synaptic transmission to RGCs in the adult retina seemed to be mediated mainly by non-NMDAR with only a minor contribution of NMDAR.
Keywords: ganglion cells • receptors: pharmacology/physiology • synapse