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The Journal of Neuroscience, January 15, 2000, 20(2):806-812

GABAC Receptors Control Adaptive Changes in a Glycinergic Inhibitory Pathway in Salamander Retina

Paul B. Cook1, Peter D. Lukasiewicz2, and John S. McReynolds1

1 Department of Physiology, The University of Michigan, Ann Arbor, Michigan, and 2 Department of Ophthalmology and Visual Science, Washington University, St. Louis, Missouri

We studied the role of GABA in adaptive changes in a lateral inhibitory system in the tiger salamander retina. In dark-adapted retinal slice preparations picrotoxin caused a slow enhancement of glycine-mediated IPSCs in ganglion cells. The enhancement of glycinergic IPSCs developed slowly over the course of 5-20 min, even though picrotoxin blocked both GABAA and GABAC receptors within a few seconds. The slow enhancement of glycinergic IPSCs by picrotoxin was much weaker in light-adapted preparations. The slow enhancement of glycinergic inhibitory inputs was not produced by bicuculline, indicating that it involved GABAC receptors. The responses of ganglion cells to direct application of glycine were not enhanced by picrotoxin, indicating that the enhancement was not caused by an action on glycine receptors. In dark-adapted eyecup preparations picrotoxin caused a slow enhancement of glycinergic IPSPs and transient lateral inhibition produced by a rotating windmill pattern, similar to the effect of light adaptation. The results suggest that the glycinergic inhibitory inputs are modulated by an unknown substance whose synthesis and/or release is inhibited in dark-adapted retinas by GABA acting at GABAC receptors.

Key words: retina; adaptation; GABAC receptor; neuromodulator; glycine; salamander


Copyright © 2000 Society for Neuroscience  0270-6474/00/202806-07$05.00/0


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