Transient ischemia increases neuronal nitric oxide synthase, argininosuccinate synthetase and argininosuccinate lyase co-expression in rat striatal neurons.
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.
Bizzoco
Elisa
E
Department of Anatomy, Histology and Forensic Medicine, Section of Histology, University of Florence, Viale G. Pieraccini, 6, 50134 Florence, Italy.
Vannucchi
Maria-Giuliana
MG
Faussone-Pellegrini
Maria-Simonetta
MS
D000818:Animals; D001123:Argininosuccinate Lyase / Q000378:metabolism*; D001124:Argininosuccinate Synthase / Q000378:metabolism*; D001157:Arterial Occlusive Diseases / Q000150:complications; D002544:Cerebral Infarction / Q000473:pathology; D003342:Corpus Striatum / Q000201:enzymology; D002546:Ischemic Attack, Transient / Q000201:enzymology* / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D008297:Male; D020768:Middle Cerebral Artery; D009420:Nervous System / Q000503:physiopathology; D009474:Neurons / Q000201:enzymology*; D052248:Nitric Oxide Synthase Type I / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000201:enzymology; D013997:Time Factors
D052248:Nitric Oxide Synthase Type I; D001123:Argininosuccinate Lyase; D001124:Argininosuccinate Synthase