Modeling Starburst Cells’ GABAB Receptors and Their Putative Role in Motion Sensitivity

Neal and Cunningham (Neal, M. J., and J. R. Cunningham. 1995. J. Physiol. (Lond.). 482:363–372) showed that GABAB agonists and glycinergic antagonists enhance the light-evoked release of retinal acetylcholine. They proposed that glycinergic cells inhibit the cholinergic Starburst amacrine cells and are in turn inhibited by GABA through GABAB receptors. However, as recently shown, glycinergic cells do not appear to have GABAB receptors. In contrast, the Starburst amacrine cell has GABAB receptors in a subpopulation of its varicosities. We thus propose an alternate model in which GABAB-receptor activation reduces the release of ACh from some dendritic compartments onto a glycinergic cell, which then feeds back and inhibits the Starburst cell. In this model, the GABA necessary to make these receptors active comes from the Starburst cell itself, making them autoreceptors. Computer simulations of this model show that it accounts quantitatively for the Neal and Cunningham data. We also argue that GABAB receptors could work to increase the sensitivity to motion over other stimuli.