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C-J Dong, WA Hare; Modulation of the Retinal ON Response by the GABAc feedback Pathway in Mammalian Retina in vivo . Invest. Ophthalmol. Vis. Sci. 2002;43(13):895.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: To demonstrate that the amplitude and kinetics of the electroretinogram (ERG) b-wave can be modulated by the GABAc receptor mediated feedback pathway and to explore the utility of the b-wave as a non-invasive tool to study temporal modulation of the retinal ON response by the GABAc and other inhibitory pathways in the mammalian retina in vivo. Methods: ERG responses were recorded from both eyes of anesthetized, dark-adapted, adult pigmented rabbits. The responses were elicited by ultra bright white (6500 OK) light-emitting diodes (LEDs), whose output was precisely controlled by a computer-controlled driver. ERG signals were band-filtered from 0.1 to 300 Hz and digitized at 4 KHz. All test compounds were applied by intravitreal injection. Results: Application of the GABAc receptor blockers, either tetrahydropyridine methylphosphinic acid (TPMPA) or picrotoxin (PTX), decreased b-wave amplitude and prolonged selectively the decay, but not the rising phase of the b-wave. This suggests that tonic activity of the GABAc pathway is low under dark-adapted conditions and that light stimulation activates the GABAc feedback that in turn enhances b-wave amplitude and accelerates the its decay. The GABAc blockers had no significant effects on the a-wave, suggesting the observed effects of these blockers are produced predominantly at synapses between amacrine and ON bipolar cells. Blocking both GABAa and glycine receptor mediated inhibition with a combination of bicuculline (or SR95531) and strychnine accelerated both the rising and decay phases of the b-wave and often enhanced the amplitude of the b-wave. The effects of these GABAa and glycine receptor antagonists were mimicked by bicuculline or SR95531, but not by strychnine, and were blocked if either TPMPA or PTX was co-applied with the GABAa and glycine antagonists. The overall effects on b-wave amplitude and kinetics produced by a combination of the GABAa and GABAc antagonists or a combination of GABAa, GABAc, and glycine receptor antagonists were very similar to those produced by application of TPMPA or PTX alone. Conclusion: Our findings indicate that the GABAc feedback pathway is an important mechanism through which GABAergic amacrine cells modulate b-wave amplitude and kinetics. Our results also suggest that this pathway is involved in temporal modulation of the retinal ON response and is itself under tonic inhibition by a GABAa pathway in the mammalian retina.
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