Abstract

We report for the first time that depletion of endogenous sources of retinal GABA by the hydrazine compound semicarbazide results in the stimulation of the rate and intensity of impulse transmission along the visual pathway. This effect was 50% more pronounced when ophthalmic drops were used in place of direct cortical administration. Depletion of retinal GABA resulted in the potentiation of the intensity of the photo-induced excitatory postsynaptic potentials arriving at the optic cortex. These effects of semicarbazide were antagonized by pretreatment with the GABA-T inhibitor amino oxyacetic acid and by GABA. We have hypothesized that GABA is probably a compensatory modulator of visual functions. The efficacy of a new route for the study of GABA in vivo and the possible clinical application of this modality have been demonstrated.

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