Induction of cytosolic NADPH-diaphorase/nitric oxide synthase in reactive microglia/macrophages after quinolinic acid lesions in the rat striatum: an electron and light microscopical study

1996 ◽  
Vol 105 (1) ◽  
pp. 81-89 ◽  
Author(s):  
Jaroslaw Calka ◽  
Gerald Wolf ◽  
Werner Schmidt
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Quinolinic Acid ◽  
Microscopical Study ◽  
Nadph Diaphorase ◽  
Rat Striatum ◽  
Reactive Microglia ◽  
Oxide Synthase

Type I nitric oxide synthase fully accounts for nadph-diaphorase in rat striatum, but not cortex

Neuroscience ◽  
1994 ◽  
Vol 62 (4) ◽  
pp. 983-987 ◽  
Author(s):  
V.N. Kharazia ◽  
H.H.H.W Schmidt ◽  
R.J. Weinberg
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Nadph Diaphorase ◽  
Rat Striatum ◽  
Type I ◽  
Oxide Synthase

scholarly journals Effects of various nitric oxide synthase inhibitors on quinolinic acid-induced neuronal injury in rats

2004 ◽  
Vol 23 (1) ◽  
pp. 11-18
Author(s):  
Ivana Vasiljevic ◽  
Marina Jovanovic ◽  
Miodrag Colic ◽  
Rosa Mihajlovic ◽  
Mirjana Djukic ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Nitric Oxide Synthase ◽  
Quinolinic Acid ◽  
Neuronal Injury ◽  
Rat Striatum ◽  
Nitric Oxide Synthase Inhibitor ◽  
Nitric Oxide Synthase Inhibitors ◽  
Synthase Inhibitor ◽  
Oxide Synthase

The aetiology of neuronal death in neurodegenerative diseases, including Huntington-s disease, is still unknown. There could be a complex interplay among altered energy metabolism, excitotoxicity and oxidative stress. Our aim was to examine the effects of intrastriatal injection of a selective inhibitor of neuronal nitric oxide synthase, 7-nitroindazole, and a non-specific potent nitric oxide synthase inhibitor, Nw-nitro-L-arginine methyl ester, in order to study the possible involvement of glutathione, an important antioxidant, in quinolinic acid-induced striatal toxicity in the rat. Unilateral administration of quinolinic acid to rat striatum in a single dose of 150 nmol/L was used as a model of Huntington-s disease. The other group of animals were pretreated with 7- nitroindazole and Nw-nitro-L-arginine methyl ester, respectively. Control groups were treated with saline solution and olive oil, respectively. Content of total glutathione, was increased in the ipsi- and contralateral striatum, forebrain cortex, basal forebrain and hippocampus in the groups treated with nitric oxid synthase inhibitors and quinolinic acid compared to the quinolinic acid-treated animals. These results support the hypothesis that oxygen free radicals contribute to excitotoxic neuronal injury, and also that nitric oxide synthase inhibitors could be potential neuroprotective agents in Huntington-s disease.

Modulation of quinolinic acid-induced depletion of striatal NADPH diaphorase and enkephalinergic neurons by inhibition of nitric oxide synthase

1999 ◽  
Vol 817 (1-2) ◽  
pp. 151-162 ◽  
Author(s):  
Bettina E. Kalisch ◽  
Khem Jhamandas ◽  
Richard J. Beninger ◽  
Roland J. Boegman
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Quinolinic Acid ◽  
Nadph Diaphorase ◽  
Oxide Synthase

Morphological analyses of NADPH-diaphorase/nitric oxide synthase positive structures in human visual cortex

1994 ◽  
Vol 23 (12) ◽  
pp. 770-782 ◽  
Author(s):  
Hans -Joachim L�th ◽  
Annelies Hedlich ◽  
Heidegard Hilbig ◽  
Ernst Winkelmann ◽  
Bernd Mayer
Keyword(s):  
Nitric Oxide ◽  
Visual Cortex ◽  
Nitric Oxide Synthase ◽  
Nadph Diaphorase ◽  
Human Visual Cortex ◽  
Oxide Synthase
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