Transporter-mediated GABA release induced by excitatory amino acid agonistis associated with GAD-67 but not GAD-65 immunoreactive cells of the primate retina

The release of GABA from amacrine and interplexiform cells after exposure t o excitatory amino acids (EAAs) agonists was investigated by immunohistoche mistry. Cebus monkey retinas were treated in vitro with 50 mu M kainate (KA ) or 5 mM L-Glutamate (L-Glu), for 30 min at 37 degrees C. The effects of t he EAAs were measured by detecting immunocytochemically the GABA remaining in the tissue after stimulation. L-Glu and KA reduced the number of GABA-im munoreactive perikarya in the innermost part of the inner nuclear layer by approximately 60% and 80% respectively, as compared to controls. The cell p rocesses in the inner plexiform layer (IPL) were restricted to only three d efined bands in the strata 1, 3 and 5, as compared to an intense and homoge neous labeling in the IPL of the untreated retinas. The effect of KA was in hibited by 100 mu M CNQX, 100 mu M NNC-711, or when Na+ was replaced by cho line. The release of GABA was Ca2+-independent, suggesting the mobilization of GABA from the cytoplasmic pool of this neurotransmitter. At least two s ubsets of retinal neurons including amacrine and interplexiform cells retai ned GABA-immunoreactivity after stimulation with EAAs, as revealed by gluta mic acid decarboxylase (GAD immunocytochemistry. Our results suggest that n on-NMDA receptor activation by KA and glutamate are associated with the eff lux of GABA from cells of the inner retina (amacrine and interplexiform cel ls). The data also show that cells containing GAD-67 released GABA via its transporter, while cells containing exclusively GAD-65 apparently did not r elease the neurotransmitter by the reversal of the transporter. (C) 2000 El sevier Science B.V. All rights reserved.