Compartmental localization of γ‐aminobutyric acid type B receptors in the cholinergic circuitry of the rabbit retina

Although many effects of γ‐aminobutyric acid (GABA) on retinal function have been attributed to GABA A and GABA C receptors, specific retinal functions have also been shown to be mediated by GABA B receptors, including facilitation of light‐evoked acetylcholine release from the rabbit retina (Neal and Cunningham [1995] J. Physiol. 482:363–372). To explain the results of a rich set of experiments, Neal and Cunningham proposed a model for this facilitation. In this model, GABA B receptor‐mediated inhibition of glycinergic cells would reduce their own inhibition of cholinergic cells. In turn, muscarinic input from the latter to the glycinergic cells would complete a negative‐feedback circuitry. In this study, we have used immunohistochemical techniques to test elements of this model. We report that glycinergic amacrine cells are GABA B receptor negative. In contrast, our data reveal the localization of GABA B receptors on cholinergic/GABAergic starburst amacrine cells. High‐resolution localization of GABA B receptors on starburst amacrine cells shows that they are discretely localized to a limited population of its varicosities, the majority of likely synaptic‐release sites being devoid of detectable levels of GABA B receptors. Finally, we identify a glycinergic cell that is a potential muscarinic receptor‐bearing target of GABA B ‐modulated acetylcholine release. This target is the DAPI‐3 cell. We propose, based on these data, a modification of the Neal and Cunningham model in which GABA B receptors are on starburst, not glycinergic amacrine cells. J. Comp. Neurol. 493:448–459, 2005. © 2005 Wiley‐Liss, Inc.