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Abstract
PURPOSE: To study the mechanisms and sites of action of the carbonic anhydrase inhibitor, acetazolamide (AZM), on the rod- and cone-mediated electroretinogram (ERG) of the dark-adapted rat. METHODS: After a within-subjects design, ERG responses to brief, full-field flashes were recorded from adult (60 to 90 days old) albino rats, with and without AZM (5 mg/100 g, intraperitoneally). Flickering stimuli (6 and 26 Hz) were used to study rod- and cone-mediated responses. Aspartate-isolated responses of the isolated retina were recorded with and without AZM in the superfusate. The a-wave and PIII responses were fitted with a model of the rod's response by estimating the maximum response (Rmp3), sensitivity (S), and delay td. The b-wave response amplitude and implicit time were examined as a function of stimulus energy. The parameters obtained in the AZM-treated and untreated conditions were compared. RESULTS: Acetazolamide causes a significant decrease in saturated rod response, b-wave amplitude, aspartate-isolated PIII, and the rod- and cone-mediated responses to flickering light. The estimated sensitivity of the rod response (S), b-wave sensitivity, and b-wave implicit time are not altered significantly by AZM. CONCLUSION: Acetazolamide, probably through mechanisms that acidify the retina, attenuates the amplitudes of the retinal responses without significant effect on sensitivity.