Journal
EXPERIMENTAL EYE RESEARCH
Volume 83, Issue 5, Pages 1135-1145Publisher
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.exer.2006.05.022
Keywords
neuroprotection; excitotoxicity; retinal ganglion cell; nicotinic acetylcholine receptor
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Funding
- NEI NIH HHS [EY 014861] Funding Source: Medline
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In the mammalian retina, excess glutamate release has been shown to be involved in retinal ganglion cell (RGC) death associated with various diseases. Recent studies have determined that activation of alpha 7 nicotinic acetylcholine receptors (nAChRs) partially protect isolated RGCs from glutamate-induced excitotoxicity. In this study, we further classify the types of nAChRs involved in neuroprotection against glutamate-induced excitotoxicity using isolated adult pig RGCs. Cells were isolated with a modified two-step immunoselective panning technique designed to isolate RGCs from other retinal neurons. Once isolated, nAChR subunits were identified using a combination of pharmacological and immunocytochemical techniques. In cell culture experiments, a variety of alpha 4 nAChR specific agonists were found to have a partial neuroprotective against glutamate-induced excitotoxicity. This neuroprotection was abolished in the presence of the alpha 4 nAChR antagonist, dihydro-beta-erythroidine (DHOE). Immunocytochemical results localized several nAChR subunits on isolated adult pig RGCs; in particular alpha 4, alpha 7 and beta 2 nAChR subunits. Large RGCs exclusively immunostained with antibodies against alpha 7 nAChR subunits whereas alpha 4 and beta 2 subunits exclusively immunostained only small RGCs. Double label experiments provided evidence that alpha 4 and beta 2 subunits co-localize on small RGCs. Knowledge of the receptor subtypes responsible for neuroprotection may lead to treatments associated with glutamate-induced excitotoxicity. (c) 2006 Elsevier Ltd. All rights reserved.
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