The inhibition of [3H]acetylcholine
(ACh) release from cholinergic amacrine cells by glycine
and GABA was studied using an in vivo eyecup preparation
in anesthetized rabbits. Glycine (1 mM) had no effect on
basal ACh release, but completely blocked the light-evoked
release of ACh. Glycine also blocked the strong potentiating
effects of picrotoxin (20 μM) normally observed on
basal and light-evoked release. Strychnine (20 μM)
increased basal release, albeit less than picrotoxin, but
partially inhibited and altered the shape of light-evoked
responses. Co-perfusion of picrotoxin and strychnine after
strychnine application resulted in a larger additional
basal increase. However, light-evoked responses were not
restored to a control shape and magnitude, or to potentiated
levels as with picrotoxin alone, but remained altered and
partially inhibited. These results support the concept
of a sustained GABA-mediated inhibition of the cholinergic
pathway in the intact retina. In contrast, glycine-mediated
inhibition of the cholinergic pathway differs, with the
present results indicating a significantly smaller sustained
inhibition of basal release and a temporal inhibition of
light-evoked release. The lack of effect of any of these
compounds on kainate-evoked responses indicates that these
effects are predominately indirect, possibly on the presynaptic
bipolar cell.