ArticleThe Journal of comparative neurology2005
Compartmental localization of gamma-aminobutyric acid type B receptors in the cholinergic circuitry of the rabbit retina.
Article in The Journal of comparative neurology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 20 citations in OpenAlex.
- Long-distance object motion evokes direction selectivity in retinal neurons through nicotinic receptors in bipolar cells.Journal of neurophysiology · 2026Article
- Cholinergic feedback to bipolar cells contributes to motion detection in the mouse retina.Cell reports · 2021Article
- Inhibitory input to the direction-selective ganglion cell is saturated at low contrast.Journal of neurophysiology · 2015Article
- Identification of GABA receptors in chick cornea.Molecular vision · 2012Article
- GABA(B) receptor feedback regulation of bipolar cell transmitter release.The Journal of physiology · 2010Article
- Muscarinic acetylcholine receptor localization and activation effects on ganglion response properties.Investigative ophthalmology & visual science · 2010Article
- Modeling Starburst cells' GABA(B) receptors and their putative role in motion sensitivity.Biophysical journal · 2006Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Although many effects of gamma-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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.