Journal
BIOPHYSICAL JOURNAL
Volume 91, Issue 2, Pages 473-486Publisher
CELL PRESS
DOI: 10.1529/biophysj.105.072256
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Funding
- NEI NIH HHS [EY11170, R01 EY008921, R01 EY007552, R01 EY011170, EY08921, EY07552] Funding Source: Medline
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Neal and Cunningham ( Neal, M. J., and J. R. Cunningham. 1995. J. Physiol. ( Lond.). 482: 363 - 372) showed that GABA(B) 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 GABA(B) receptors. However, as recently shown, glycinergic cells do not appear to have GABA(B) receptors. In contrast, the Starburst amacrine cell has GABA(B) receptors in a subpopulation of its varicosities. We thus propose an alternate model in which GABA(B)-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 GABA(B) receptors could work to increase the sensitivity to motion over other stimuli.
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