Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
9191864 | Experimental Neurology | 2005 | 11 Pages |
Abstract
Calcium-independent nitric oxide synthase (NOS) activity has been reported in ischemic brains and usually attributed to the inducible isoform, iNOS. Because calcium-independent mechanisms have recently been shown to regulate the constitutive calcium-dependent NOS, we proposed to confirm the presence of iNOS activity in our model of transient focal cerebral ischemia in rats. Our initial results showed that, in our model, ischemia induced an important increase in brain calcium concentration. Consequently, the determination of calcium-independent NOS activity required a higher concentration of calcium chelator than classically used in the NOS assay. In these conditions, calcium-independent NOS activity was not observed after ischemia. Moreover, our ischemia was associated with neither iNOS protein expression, measured by Western blotting, nor increased NO production, evaluated by its metabolites (nitrate/nitrite). Our results demonstrate that iNOS activity may be overestimated due to increased brain calcium concentration in ischemic conditions and also that iNOS is not systematically induced after cerebral ischemia.
Keywords
LPSinducible NO-synthaseEndothelial NO-synthasenNOSeNOSiNOSNOSCCATBSMCA1400WDMSONOxTransient focal cerebral ischemiaTris-buffered salinestandard error of meanDimethyl sulfoxydeinducible nitric oxide synthasemiddle cerebral arterycommon carotid arterylipopolysaccharideSEMNitrites/nitratesNitric oxidenitric oxide synthase
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Authors
Dominique Lerouet, Mehrnaz Jafarian-Tehrani, Gaëlle Louin, Bruno Palmier, Dominique Bonnefont-Rousselot, Michel Plotkine, Isabelle Margaill,