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Titolo:
Sustained, long-lasting inhibition of nitric oxide synthase aggravates theneural damage in some models of excitotoxic brain injury
Autore:
Ciani, E; Baldinotti, I; Contestabile, A;
Indirizzi:
Univ Bologna, Dept Biol, I-40126 Bologna, Italy Univ Bologna Bologna Italy I-40126 na, Dept Biol, I-40126 Bologna, Italy
Titolo Testata:
BRAIN RESEARCH BULLETIN
fascicolo: 1, volume: 56, anno: 2001,
pagine: 29 - 35
SICI:
0361-9230(20010901)56:1<29:SLIONO>2.0.ZU;2-M
Fonte:
ISI
Lingua:
ENG
Soggetto:
FOCAL CEREBRAL-ISCHEMIA; KAINATE-INDUCED SEIZURES; IN-VIVO; KAINIC ACID; RECEPTOR ANTAGONIST; NEURONAL MESSENGER; NERVOUS-SYSTEM; NMDA RECEPTOR; NO SYNTHASE; BLOOD-FLOW;
Keywords:
neurodegeneration; neuroprotection; L-NAME; rat; striatum; nucleus basalis magnocellularis;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
62
Recensione:
Indirizzi per estratti:
Indirizzo: Contestabile, A Univ Bologna, Dept Biol, Via Selmi 3, I-40126 Bologna, Italy Univ Bologna Via Selmi 3 Bologna Italy I-40126 gna, Italy
Citazione:
E. Ciani et al., "Sustained, long-lasting inhibition of nitric oxide synthase aggravates theneural damage in some models of excitotoxic brain injury", BRAIN RES B, 56(1), 2001, pp. 29-35

Abstract

Brain nitric oxide (NO) can be a mediator of physiological and neuroprotective actions and an effector of neural damage. The effectiveness of acute or chronic inhibition of NO production in in vivo experiments of neurotoxicity/neuroprotection is controversial. We report here on the effects of a chronic, sustained inhibition of nitric oxide synthase (NOS) on the neurodegenerative damage caused by three different excitotoxic lesions. The damage caused by intrastriatal injection of ibotenic or kainic acid was aggravated in rats subjected to chronic NOS inhibition. On the contrary, the drop of cortical cholinergic input consequent to ibotenic acid-mediated degeneration of basal forebrain neurons was not altered by chronic NOS inhibition. The worsening of the damage was not related to any overt differential sensitivity to excitotoxicity of NOS-containing striatal neurons under conditions of NOS inhibition. These results suggest that, contrary to what has been oftenreported for short-term, mild inhibition of NO production, chronic and sustained NOS inhibition may exacerbate neuropathology. Thus, long-lasting shortage of NO may be detrimental when neuroprotective mechanisms related to the physiological action of this free radical are severely impaired. Although we cannot exclude that inhibition of the endothelial NOS isoform could have contributed to the worsening of neuropathology, differences among the paradigms of neurotoxicity used in the present study suggest a primary involvement of the neuronal NOS isoform. In view of the potential therapeutic useof NOS inhibitors, the effects of a too drastic alteration of the balance between neuroprotective and neurodegenerative actions of NO should be carefully considered. (C) 2001 Elsevier Science Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/04/20 alle ore 21:01:37