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.