Please use this identifier to cite or link to this item: https://hdl.handle.net/20.500.12202/3782
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dc.contributor.authorWexler, Eric Michael
dc.date.accessioned2018-07-12T18:54:13Z
dc.date.available2018-07-12T18:54:13Z
dc.date.issued1998
dc.identifier.citationSource: Dissertation Abstracts International, Volume: 59-06, Section: B, page: 2610.;Advisors: Scott Nawy.
dc.identifier.urihttps://ezproxy.yu.edu/login?url=http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqm&rft_dat=xri:pqdiss:9838262
dc.identifier.urihttps://hdl.handle.net/20.500.12202/3782
dc.description.abstractWe prepared dissociated rat retinal cultures, determining the conditions necessary for survival of all major classes of neuron as well as several amacrine cell subtypes. These cell types were distinguishable immunohistochemically, electrophysiologically and morphometrically. Using this model system, we demonstrated that: (A) BDNF promotes survival of rod bipolar cells by binding Muller cell p75 receptors and subsequent release of FGF-2. (B) Nitric Oxide depresses amacrine cell GABA{dollar}\rm\sb{lcub}A{rcub}{dollar} receptors through two separate, but convergent cGMP-dependent pathways. These are (1) direct PKG-mediated receptor depression, and (2) indirect depotentiation of the receptor by PDE II-mediated down-regulation of PKA, as a result of increased cAMP hydrolysis.
dc.publisherProQuest Dissertations & Theses
dc.subjectNeurosciences.
dc.subjectOphthalmology.
dc.titlePhysiology and development of cultured mammalian retinal interneurons
dc.typeDissertation
Appears in Collections:Albert Einstein College of Medicine: Doctoral Dissertations

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