Figure 8.

Postsynaptic buffering of Ca²⁺ or blocking CB1 receptors abolishes synaptic depression at CBC6 to α On RGC synapse. (A) Responses from an α On RGCs to paired, 1 ms stimuli at the stimulus intervals (*timing of stimulus). The internal solution contained 20 mM BAPTA. (B) Responses of an α On RGCs to paired, 1 ms stimuli as in (A) with 2 μM AM251 added to the bathing solution. Summary plot of the PPR under the conditions shown in (A,B). Cells recorded with the internal solution containing BAPTA and AM251 are from the retina with normal IOP but were induced to undergo NMDA-dependent plasticity by omitting D-APV. Only α On RGCs that displayed significant rectification [rectification index (RI) < 0.4] were included for analysis. (C) Time course of recovery from PPD in α On RGCs recorded with BAPTA in the pipet solution, or with EGTA in the pipet and AM251 in the bath. PPD decreased monotonically, with no evidence of a delayed increase in depression despite significant expression of CP-AMPARs in these cells. (D) Statistical comparison of PPR at an interval of 200 ms in cells recorded with EGTA (a group of α On RGCs from Figure 7C), BAPTA, or with AM-251 in the bath. (E) Recordings showing paired-pulse responses (interval of 100 ms) from an α On RGC at the indicated voltages. The stimulus intensity was reduced five fold from the intensity used for paired-pulse recordings presented previously. (F) Recordings from (E) scaled to show the increase in PPD at positive voltage. (G) Population data from α On RGCs (n = 13) timing of stimulus.