Amacrine cells that respond transiently to maintained illumination are thought to mediate transient inhibitory input to
ganglion cells. The excitation of these transient amacrine cells is thought to be limited by inhibitory feedback to bipolar cells. We investigated the possibility that desensitizing
AMPA and/or
kainate (KA) receptors on amacrine cells might also limit the duration of amacrine cell excitation. To determine how these receptors might affect amacrine cell input and output, we made whole-cell recordings from amacrine and
ganglion cells in the salamander
retinal slice. The specific
AMPA receptor antagonist
GYKI-53655 blocked non-
NMDA receptor-mediated amacrine cell excitatory postsynaptic currents (EPSCs) and
kainate puff-elicited currents, indicating that
AMPA, and not KA, receptors mediated the responses.
Cyclothiazide, an agent that reduces
AMPA receptor desensitization, increased the amplitude and duration of amacrine cell EPSCs. To measure the output of transient amacrine cells, we recorded glycinergic inhibitory postsynaptic currents (IPSCs) from
ganglion cells, and found that these were also enhanced by
cyclothiazide. Thus, prolongation of amacrine cell
AMPA receptor activation enhanced amacrine cell output. Current responses elicited by puffing
glycine onto
ganglion cell dendrites were not affected by
cyclothiazide, indicating that the enhancement of glycinergic IPSCs was not due to a direct effect on
glycine receptors. These data suggest that rapid
AMPA receptor desensitization and/or deactivation limits glycinergic amacrine cell excitation and the resulting inhibitory synaptic output.