Lack of iNOS induction in a severe model of transient focal cerebral ischemia in rats.

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.

journal_name

Exp Neurol

journal_title

Experimental neurology

authors

Lerouet D,Jafarian-Tehrani M,Louin G,Palmier B,Bonnefont-Rousselot D,Plotkine M,Margaill I

doi

10.1016/j.expneurol.2005.05.001

keywords:

subject

Has Abstract

pub_date

2005-09-01 00:00:00

pages

218-28

issue

1

eissn

0014-4886

issn

1090-2430

pii

S0014-4886(05)00170-6

journal_volume

195

pub_type

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