Abstract
High‐affinity uptake, potassium‐stimulated release and receptor binding of γ‐aminobutyric acid (GABA) and taurine were studied in retinas of rats treated with monosodium glutamate (MSG) or iodoacetate‐malate (IAM). Such treatments produce a selective damage of the inner retinal layers (MSG) or of the photoreceptor layer (IAM).
MSG treatment decreased GABA uptake by more than 60%. Also, the potassium‐stimulated release of this amino acid was markedly diminished (90%) in retinas lesioned by MSG. MSG treatment decreased ^3^H‐GABA binding by 45%. Uptake, release or binding of GABA were unaffected by IAM‐treatment.
Taurine uptake was reduced by a similar degree by both MSG and IAM treatment, 57% and 38% respectively. Potassium‐stimulated release of taurine was unchanged by MSG and 50% reduced by IAM. Both treatments reduced the spontaneous release of endogenous taurine. Binding of taurine to receptors in retinal membranes was practically unaffected by any of the treatments utilized.
These results are consistent with a neurotransmitter action of GABA at the inner retinal layers, while they do not support a major role for taurine as a synaptic transmitter in retina.