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Titolo:
The influence of CGP-40116 on bicuculline evoked seizures in mice exposed to transient episode of brain oligemia
Autore:
Rejdak, K; Rejdak, R; Czuczwar, SJ; Kleinrok, Z; Sieklucka-Dziuba, M;
Indirizzi:
Med Univ, Dept Hyg, PL-20080 Lublin, Poland Med Univ Lublin Poland PL-20080 Univ, Dept Hyg, PL-20080 Lublin, Poland Med Univ, Dept Pharmacol, PL-20080 Lublin, Poland Med Univ Lublin PolandPL-20080 Dept Pharmacol, PL-20080 Lublin, Poland Inst Agr Med, Isotope Lab, PL-20080 Lublin, Poland Inst Agr Med Lublin Poland PL-20080 Isotope Lab, PL-20080 Lublin, Poland
Titolo Testata:
JOURNAL OF NEURAL TRANSMISSION
fascicolo: 11, volume: 107, anno: 2000,
pagine: 1263 - 1272
SICI:
0300-9564(2000)107:11<1263:TIOCOB>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
INDUCED NEURONAL DAMAGE; ISCHEMIC TOLERANCE; STATUS EPILEPTICUS; RECEPTOR ANTAGONISTS; GERBIL HIPPOCAMPUS; CEREBRAL-ISCHEMIA; TEMPORAL PROFILE; CORTICAL-NEURONS; RAT-BRAIN; INDUCTION;
Keywords:
CGP-40116; pilocarpine; GABA; ischemia; seizures; preconditioning;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
38
Recensione:
Indirizzi per estratti:
Indirizzo: Rejdak, K Med Univ, Dept Hyg, 11 Radziwillowska Str, PL-20080 Lublin, Poland Med Univ 11 Radziwillowska Str Lublin Poland PL-20080 n, Poland
Citazione:
K. Rejdak et al., "The influence of CGP-40116 on bicuculline evoked seizures in mice exposed to transient episode of brain oligemia", J NEURAL TR, 107(11), 2000, pp. 1263-1272

Abstract

To assess the role of NMDA receptors in the modulation of a brain tolerance after a transient cerebral mild ischemia, adult mice were exposed for 30 min to bilateral clamping of the common carotid arteries (BCCA) under pentobarbital anaesthesia. The competitive NMDA antagonist CGP-40116 was administered intraperitoneally (IP) in two experimental paradigms: a) acute treatment: twice, 4.0 mg/kg; 1,5 hour before the clamping of vessels and 6 hours after re-circulation and b) chronic treatment in a dose of 1.0 mg/kg; started 24 hours after re-circulation and continued once daily for 13 days with the last injection 24 hours before the induction of convulsions. Seizures were evoked with bicuculline (3.5 mg/kg, IF) 14 days after BCCA. Transient brain oligemia induced protection against bicuculline toxicity. The acute treatment with CGP-40116 only partially diminished the anticonvulsant phenomenon. In contrast, the chronic treatment with the drug markedly potentiated the effect. It can be concluded that NMDA receptors only partially participate in the induction of a protective effect against bicuculline toxicity after BCCA. The chronic treatment with low doses of the NMDA antagonist may enhance the brain tolerance, possibly due to the chemical preconditioning.

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Documento generato il 01/04/20 alle ore 01:21:29