Potentiation of quinolinate-induced hippocampal lesions by inhibition of NO synthesis
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The Role of nitric oxide in convulsions induced by lindane in rats
2011, Food and Chemical ToxicologyCitation Excerpt :n-nitro-l-arginine methyl ester (L-NAME) is non-selective NOS inhibitor commonly used to decrease NO levels. Since pronconvulsive (Kim et al., 1997; Mülsch et al., 1994; Van Leeuwen et al., 1995) as well as anticonvulsive properties (Haberny et al. 1992; Hrncic et al., 2010; Rondouin et al., 1992; Rondouin et al., 1993) of NO has been reported, the role of NO in epileptogenesis is contradictory. The role of NO in lindane effects is still not investigated.
Amino acid levels in some brain areas of inducible nitric oxide synthase knock out mouse (iNOS<sup>-/-</sup>) before and after pentylenetetrazole kindling
2006, Pharmacology Biochemistry and BehaviorOxidative stress in anticholinesterase-induced excitotoxicity
2006, Toxicology of Organophosphate & Carbamate CompoundsOxidative Stress in Anticholinesterase-Induced Excitotoxicity
2005, Toxicology of Organophosphate and Carbamate CompoundsInvolvement of nitric oxide in kainic acid-induced excitotoxicity in rat brain
2002, Brain ResearchCitation Excerpt :For example, increases of nitric oxide (NO) by seizure-producing concentrations of glutamatergic receptor agonists [4,43,48], and AChE inhibitors have been demonstrated [1,30,33,35,37]. Conversely, the results of studies using nitric oxide synthase (NOS) inhibitors indicate that NO may play a role as an endogenous anticonvulsant substance [14,32,40,55]. Other reports show that administration of the NOS inhibitor N-nitro-l-arginine methylester (l-NAME) prevented limbic seizures and related hippocampal damage by tacrine (an anticholinesterase agent) in rats, but not seizures and hippocampal damage caused by KA [2,3].