Transient changes in retinal oxygen in response to light stimuli were studied to further understand the light-evoked change in oxygen consumption. Double-barreled microelectrodes, which measured oxygen and local voltage simultaneously, were positioned near the photoreceptor inner segments of the toad neural retina-retinal pigment epithelium--choroid preparation. Light-evoked oxygen responses were measured in a normal [Na ÷] solution, and in a test solution with lowered extracellular [Na ÷] to inhibit Na*/K * pumping. Under the normal [Na+] condition, retinal oxygen tension increased in response to light indicating that oxygen utilization had decreased. When the Na ÷ concentration was lowered in the retina, the oxygen tension decreased in response to light, indicating an increase in oxygen utilization which was smaller than the Na÷/K ÷ pump effect and therefore masked under normal conditions, The increase in oxygen utilization in lowered [Na ÷] was suppressed by adding 0-7 mM 3-isobutyl-l-methyl-xanthine, a phosphodiesterase inhibitor, suggesting that the response was largely due to hydrolysis and subsequent resynthesis of cyclic GMP. Results of fitting the light-evoked responses to exponential functions suggested that the decrease in oxygen consumption caused by slowing of the photoreceptor Na+/K ÷ ATPase had a time constant between 130 and 180 sec and that the increase in oxygen utilization from increased cyclic GMP synthesis was faster.

1. Changes in intracellular calcium concentration [Ca2+]i in response to extracellularly applied gamma‐aminobutyric acid (GABA) were studied in isolated horizontal cells from the all‐rod skate retina. 2. Calcium measurements were made using fura‐2 AM, both with and without whole‐cell voltage clamp. Superfusion with GABA, in the absence of voltage clamp, resulted in an increase in [Ca2+]i; the threshold for detection was approximately 50 microM GABA, and a maximal response was elicited by 500 microM GABA. 3. The rise in [Ca2+]i was not mimicked by baclofen nor was it blocked by phaclofen, picrotoxin or bicuculline. However, the GABA‐induced [Ca2+]i increase was completely abolished when extracellular sodium was replaced with N‐methyl‐D‐glucamine. 4. With the horizontal cell voltage clamped at ‐70 mV, GABA evoked a large inward current, but there was no concomitant change in [Ca2+]i. Nifedipine, which blocks L‐type voltage‐gated Ca2+ channels, suppressed the GABA‐induced increase in [Ca2+]i. These findings suggest that the calcium response was initiated by GABA activation of sodium dependent electrogenic transport, and that the resultant depolarization led to the opening of voltage‐gated Ca2+ channels, and a rise in [Ca2+]i. 5. The GABA‐induced influx of calcium appears not to have been the sole source of the calcium increase. The GABA‐induced rise in [Ca2+]i was reduced by dantrolene, indicating that internal Ca2+ stores contributed to the GABA‐mediated Ca2+ response. 6. These observations demonstrate that activation of the GABA transporter induces changes in [Ca2+]i which may have important implications for the functional properties of horizontal cells.

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