Evidence for bidirectional changes in nitric oxide synthase activity in the rat striatum after excitotoxically (quinolinic acid) induced degeneration

Neuroscience
W SchmidtH H Schmidt

Abstract

Nitric oxide, a gaseous inter- and intracellular messenger, is thought to mediate neurotoxicity via excitatory amino acid receptors which may contribute to the pathogenesis of a variety of neuronal diseases. Excitotoxin lesions induced by quinolinic acid were made unilaterally in the rat striatum to study biochemically, light- and electron microscopically the possible involvement of the nitric oxide synthesizing enzyme nitric oxide synthase in degeneration processes. 5 days after quinolinic acid injection nitric oxide synthase activity in the striatum was elevated to 196.5% (P < 0.005% as compared to controls). There was no requirement of Ca2+ for the enzyme activity measured indicating that the elevation is due to the inducible isoform of nitric oxide synthase. Parallel to the depletion of neurons by quinolinic acid a massive gliosis was seen. Whereas quiescent astroglial cells in the normal striatum did not show any light microscopically detectable nicotinamide adenine dinucleotide phosphate diaphorase reaction, reactive astroglia revealed a substantial labeling distributed over the cell body and their stellar processes. Within the lesion and, particularly, close to the needle tract the number of microglia/macrophages labeled...Continue Reading

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Citations

Jan 11, 2005·Neurotoxicity Research·Gilles J GuilleminBruce J Brew
Jun 24, 1999·Journal of Neuroscience Methods·A StanariusG Wolf
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Jul 12, 2002·Journal of Neuroscience Research·Laia AcarinBernardo Castellano
Apr 28, 2006·Journal of Neurochemistry·Alessio MetereA M Michela Di Stasi

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