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Titolo:
Effects of thienylphencyclidine (TCP) on seizure activity and brain damageproduced by soman in guinea-pigs: ECoG correlates of neurotoxicity
Autore:
Carpentier, P; Foquin, A; Kamenka, JM; Rondouin, G; Lerner-Natoli, M; de Groot, DMG; Lallement, G;
Indirizzi:
Ctr Rech, Serv Sante Armees, Unite Neurotoxicol, F-38702 La Tronche, France Ctr Rech La Tronche France F-38702 rotoxicol, F-38702 La Tronche, France Ecole Natl Super Chim Montpellier, CNRS, UPR 8402, INSERM,U249, F-34053 Montpellier 1, France Ecole Natl Super Chim Montpellier Montpellier France 1 pellier 1, France CNRS, INSERM, Inst Biol, UPR 8402,U249, F-34060 Montpellier, France CNRS Montpellier France F-34060 R 8402,U249, F-34060 Montpellier, France TNO, Nutr & Food Res Inst, NL-3700 AJ Zeist, Netherlands TNO Zeist Netherlands NL-3700 AJ Res Inst, NL-3700 AJ Zeist, Netherlands
Titolo Testata:
NEUROTOXICOLOGY
fascicolo: 1, volume: 22, anno: 2001,
pagine: 13 - 28
SICI:
0161-813X(200102)22:1<13:EOT(OS>2.0.ZU;2-H
Fonte:
ISI
Lingua:
ENG
Soggetto:
NICOTINIC ACETYLCHOLINE-RECEPTOR; STATUS-EPILEPTICUS; KAINIC ACID; HIPPOCAMPAL DAMAGE; GACYCLIDINE GK-11; CEREBRAL-CORTEX; NMDA RECEPTOR; MK-801; ANTICONVULSANT; PHENCYCLIDINE;
Keywords:
soman; atropine sulphate; pyridostigmine; TCP; ECoG; seizure activity; ECoG power spectrum; brain damage; guinea-pig;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
54
Recensione:
Indirizzi per estratti:
Indirizzo: Carpentier, P Ctr Rech, Serv Sante Armees, Unite Neurotoxicol, BP 87, F-38702 La Tronche, France Ctr Rech BP 87 La Tronche France F-38702 La Tronche, France
Citazione:
P. Carpentier et al., "Effects of thienylphencyclidine (TCP) on seizure activity and brain damageproduced by soman in guinea-pigs: ECoG correlates of neurotoxicity", NEUROTOXICO, 22(1), 2001, pp. 13-28

Abstract

The capacity of thienylcyclohexylpiperidine (TCP), a non-competitive blocker of the N-methyl-D-aspartate (NMDA) receptor, to counteract the convulsant, lethal, and neuropathological effects of 2 x LD50 of soman (an irreversible inhibitor of cholinesterase) was investigated in guinea-pigs treated bypyridostigmine and atropine sulphate. The effects of a weak dose of TCP (1mg/kg) used in the present study globally reproduced those previously obtained with a higher dose (2.5 mg/kg; [Neurotoxicology 15 (1994) 837])1 TCP was again most protective when given curatively within the first hour of soman-induced seizures, in this condition, (a) paroxysmal activity ceased in 10-20 min, (b) all the animals survived, (c) the majority of them recovered remarkably well and did not show any brain damage 24 h after the intoxication, and (d) the minimal duration of seizure activity normally required for producing soman-induced brain damage in other pharmacological environments was increased from 10 to 40 min to 80 min. Strikingly, when TCP was given 120 min after seizure onset, it failed to show any anticonvulsant activity but still provided neuroprotection in the hippocampus. The present study also gives additional evidence (see [Neurotoxicology 21 (4) (2000) 521]) that in soman poisoning, (a) the development of brain damage depends on the occurrence of ECoG seizures, (b) the topographical distribution of lesions depends on seizure duration, and (c) an increase of the relative power in the lowest (delta) frequency band might be a reliable marker of neuronal degradation. All these findings confirm that (a) glutamatergic NMDA receptors are involved in the mechanisms of soman-induced seizures and brain damage, (b) non-competitive antagonists of NMDA receptors might be promising candidatesfor post-treatment of soman poisoning, and (c) ECoG parameters from ECoG tracings and power spectrum might serve as useful external predictors for soman-induced neuropathological changes. (C) 2001 Elsevier Science Inc. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/03/20 alle ore 12:12:39