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Titolo:
The effect of CGP-40116 on pilocarpine evoked seizures in mice exposed to transient episode of brain ischemia
Autore:
Rejdak, K; Rejdak, R; Stelmasiak, Z; 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-20090 Lublin, Poland Med Univ Lublin PolandPL-20090 Dept Pharmacol, PL-20090 Lublin, Poland Med Univ, Dept Neurol, PL-20090 Lublin, Poland Med Univ Lublin Poland PL-20090 iv, Dept Neurol, PL-20090 Lublin, Poland Inst Agr Med, Isotope Lab, PL-20950 Lublin, Poland Inst Agr Med Lublin Poland PL-20950 Isotope Lab, PL-20950 Lublin, Poland
Titolo Testata:
EPILEPSY RESEARCH
fascicolo: 3, volume: 41, anno: 2000,
pagine: 213 - 222
SICI:
0920-1211(200010)41:3<213:TEOCOP>2.0.ZU;2-T
Fonte:
ISI
Lingua:
ENG
Soggetto:
INDUCED NEURONAL DAMAGE; RAT-BRAIN; STATUS EPILEPTICUS; CEREBRAL-ISCHEMIA; RECEPTOR ANTAGONISTS; RETROSPLENIAL CORTEX; GERBIL HIPPOCAMPUS; FOREBRAIN ISCHEMIA; CAROTID ARTERIES; TEMPORAL PROFILE;
Keywords:
CGP-40116; pilocarpine; GABA; ischemia; seizures; preconditioning;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
49
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 effect of CGP-40116 on pilocarpine evoked seizures in mice exposed to transient episode of brain ischemia", EPILEPSY R, 41(3), 2000, pp. 213-222

Abstract

The objective of the study was to examine the role of N-methyl-D-aspartate(NMDA) receptors in the modulation of a brain tolerance after a transient cerebral ischemia. Adult mice were exposed for 30 min to bilateral clampingof common carotid arteries (BCCA) under anaesthesia. The competitive NMDA antagonist CGP-40116 was administered intraperitoneally (i.p.) in two experimental paradigms, (a) acute treatment: twice, 4.0 mg/kg; 1.5 h before the clamping of vessels and 6 h after re-circulation and (b) chronic treatment in a dose of 1.0 mg/kg; started 24 h after re-circulation and continued once daily for 13 days with the last injection 24 h before the induction of convulsions. Seizures were evoked with pilocarpine (400 mg/kg, i.p.) 14 days after BCCA. The preliminary study showed that BCCA induced protection against pilocarpine toxicity. The acute treatment with CGP-40116 partially diminished the anticonvulsant phenomenon. In contrast, the chronic treatment with the drug led to a marked potentiation of the effect. The whole brain gamma-arninobutyric acid (GABA) analysis performed 14 days after BCCA showed a moderate increase in vehicle-treated mice and a significant elevation afterchronic treatment with CGP-40116. It can be concluded that NMDA antagonists may exert the opposite effects on the brain tolerance against pilocarpinetoxicity after BCCA. The acute treatment with CGP-40116 diminished its induction while the chronic low-dose treatment enhanced a brain tolerance, possibly through the mechanism of chemical preconditioning. (C) 2000 Elsevier Science B.V. All rights reserved.

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Documento generato il 05/04/20 alle ore 05:56:42