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pubmed-article:9682841pubmed:abstractTextAspirin is widely used as an analgesic, in the secondary prevention of stroke, and has recently been suggested to be a putative neuroprotective agent, yet whether it acts directly on the central nervous system (CNS) is not yet clarified. We therefore examined the effect of lysine acetylsalicylate (L-ASA, 4-2000 microM) on neuronal function under normal conditions and following 1 h of ischemia using the in vitro rabbit retina preparation. L-ASA inhibited the light-evoked compound action potentials, but not the electroretinogram, in a concentration-dependent manner. In addition, L-ASA (2000 microM, but not 4, 40 or 200 microM) administered during ischemia, reduced the recovery of neuronal function compared to control (untreated) retinas. L-ASA therefore inhibits CNS neurotransmission, but not phototransduction, in a concentration-dependent manner. In addition, high concentration L-ASA impairs the recovery of neuronal function following an ischemic episode.lld:pubmed
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pubmed-article:9682841pubmed:pagination159-62lld:pubmed
pubmed-article:9682841pubmed:dateRevised2008-11-21lld:pubmed
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pubmed-article:9682841pubmed:articleTitleAcetylsalicylate administered during simulated ischemia reduces the recovery of neuronal function in the in vitro rabbit retina.lld:pubmed
pubmed-article:9682841pubmed:affiliationNeurosurgical Service, Massachusetts General Hospital and Harvard Medical School, Boston 02114, USA. Maynard@helix.mgh.harvard.edulld:pubmed
pubmed-article:9682841pubmed:publicationTypeJournal Articlelld:pubmed
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pubmed-article:9682841pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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