dc.creatorUlmer H.J.
dc.creatorFernandes de Lima V.M.
dc.creatorHanke W.
dc.date1995
dc.date2015-06-26T17:14:45Z
dc.date2015-11-26T14:20:31Z
dc.date2015-06-26T17:14:45Z
dc.date2015-11-26T14:20:31Z
dc.date.accessioned2018-03-28T21:22:12Z
dc.date.available2018-03-28T21:22:12Z
dc.identifier
dc.identifierBrain Research. , v. 691, n. 1-2, p. 239 - 242, 1995.
dc.identifier68993
dc.identifier10.1016/0006-8993(95)00737-B
dc.identifierhttp://www.scopus.com/inward/record.url?eid=2-s2.0-0029096928&partnerID=40&md5=7ea1c0253b0c8eb3c711724de5ffc753
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/95997
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/95997
dc.identifier2-s2.0-0029096928
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1244272
dc.descriptionThe retinal spreading depression has been used as a tool to investigate the action of nitric oxide (NO) as a diffusible neurotransmitter which in many cases acts by raising the cGMP level in target cells. The role of NO as a vasodilating agens has been well-established and it has been suggested that the vasodilatation concurrent with cortical SD may be mediated by NO. In this study, we present pure neuronal effects of NO on SD as the chicken retina is void of bloodvessels. We show that NO directly decreases the velocity of retinal SD waves in a concentration-and time-dependent manner. This effect can be partially mimicked by application of membrane-permeable cGMP derivatives. Furthermore, a NO-mediated speed up of the recovery of the intrinsic optical signal after the wave-front is shown. © 1995.
dc.description691
dc.description1-2
dc.description239
dc.description242
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dc.languageen
dc.publisher
dc.relationBrain Research
dc.rightsfechado
dc.sourceScopus
dc.titleEffects Of Nitric Oxide On The Retinal Spreading Depression
dc.typeArtículos de revistas


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