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Transient ischemia increases neuronal nitric oxide synthase, argininosuccinate synthetase and argininosuccinate lyase co-expression in rat striatal neurons.

Abstract
In neurodegenerative diseases, an increased number of neuronal nitric oxide synthase (nNOS)-positive neurons was reported, but nothing is known on which are the neurons induced to express nNOS. Argininosuccinate synthetase (ASS), argininosuccinate lyase (ASL) and nNOS act in the L-arginine-NO-L-citrulline cycle permitting a correct NO production. In the brain, nNOS-positive neurons co-expressing ASS were known, while those co-expressing ASL were not demonstrated. We investigated by immunohistochemistry the presence of these types of neurons in the rat striatum to verify whether there was a correlation between their changes due to neurotoxic insults and animal survival. Transient ischemia, a neurodegenerative insult model, was induced in rat brain by 2 h of middle cerebral artery occlusion. The striatum, the core of ischemia, was examined at 24, 72 and 144 h after reperfusion and compared with that of rats in normal condition. ASS, ASL and nNOS-positive neurons, some of the latter also expressing ASS and ASL, were present both in normal and ischemic conditions. At 24 h after reperfusion, the number of the nNOS-positive neurons and the percentage of those co-expressing ASS and ASL were significantly increased in the animals with a longer survival and at 144 h after ischemia there was an almost complete restore of the number and/or percentage of these neurons. We hypothesize that the neurons induced to express nNOS were the ASS- and ASL-positive ones and that the neurons co-expressing nNOS, ASS and ASL, since having the enzymes necessary to maintain a correct NO production, might protect from neurotoxic insults.
AuthorsElisa Bizzoco, Maria-Giuliana Vannucchi, Maria-Simonetta Faussone-Pellegrini
JournalExperimental neurology (Exp Neurol) Vol. 204 Issue 1 Pg. 252-9 (Mar 2007) ISSN: 0014-4886 [Print] United States
PMID17198704 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Nitric Oxide Synthase Type I
  • Argininosuccinate Lyase
  • Argininosuccinate Synthase
Topics
  • Animals
  • Argininosuccinate Lyase (metabolism)
  • Argininosuccinate Synthase (metabolism)
  • Arterial Occlusive Diseases (complications)
  • Cerebral Infarction (pathology)
  • Corpus Striatum (enzymology)
  • Ischemic Attack, Transient (enzymology, etiology, metabolism, physiopathology)
  • Male
  • Middle Cerebral Artery
  • Nervous System (physiopathology)
  • Neurons (enzymology)
  • Nitric Oxide Synthase Type I (metabolism)
  • Rats
  • Rats, Wistar
  • Reperfusion Injury (enzymology)
  • Time Factors

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