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