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Titolo:
Pharmacological characterization of locomotor sensitization induced by chronic phencyclidine administration
Autore:
Phillips, M; Wang, C; Johnson, KM;
Indirizzi:
Univ Texas, Med Branch, Dept Pharmacol & Toxicol, Galveston, TX 77555 USA Univ Texas Galveston TX USA 77555 acol & Toxicol, Galveston, TX 77555 USA Univ Texas, Med Branch, Dept Psychiat & Behav Sci, Galveston, TX 77555 USAUniv Texas Galveston TX USA 77555 at & Behav Sci, Galveston, TX 77555 USA
Titolo Testata:
JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
fascicolo: 3, volume: 296, anno: 2001,
pagine: 905 - 913
SICI:
0022-3565(200103)296:3<905:PCOLSI>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
NMDA-ANTAGONIST NEUROTOXICITY; INDUCED STEREOTYPED BEHAVIOR; RAT RETROSPLENIAL CORTEX; HEAT-SHOCK GENE; DOPAMINE D-1; NEURONS; CLOZAPINE; RECEPTORS; INDUCTION; COCAINE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
43
Recensione:
Indirizzi per estratti:
Indirizzo: Johnson, KM Univ Texas, Med Branch, Dept Pharmacol & Toxicol, Galveston, TX 77555 USA Univ Texas Galveston TX USA 77555 ol, Galveston, TX 77555 USA
Citazione:
M. Phillips et al., "Pharmacological characterization of locomotor sensitization induced by chronic phencyclidine administration", J PHARM EXP, 296(3), 2001, pp. 905-913

Abstract

Phencyclidine (PCP) administration in rats acutely in high doses or chronically in lower doses causes neurotoxicity characterized by neuronal vacuolization and apoptotic neuronal death, respectively. The purpose of this study was to determine whether drugs that previously had been reported to prevent either type of neurotoxicity were also able to prevent locomotor sensitization following chronic PCP administration. PCP (5 or 20 mg/kg) was administered once a day for 5 days following drug pretreatment. After withdrawal,rats were challenged with 3.2 mg/kg PCP and locomotor activity was assessed. Haloperidol and clozapine significantly attenuated sensitization elicited by PCP (20 mg/kg). The D-1-like antagonist SCH23390 was much less effective than clozapine, showing a marginal inhibition. Risperidone, a D-2/serotonin (5-HT2) antagonist, also resulted in a marginal attenuation of 15%. Ketanserin, a 5-HT2 antagonist, had no effect. Atropine retarded sensitizationby 35% and (1)-sulpiride caused a 50% reduction. The AMPA/kainate antagonist, 6,7-dinitroquinoxaline-2,3-dione, had no effect, but barbital sodium reduced sensitization by 54%. These data suggest that gamma -aminobutyric acid A, D-2, and muscarinic receptors play a major role in the complex pathwayunderlying sensitization to PCP, whereas D-1, 5-HT2 and AMPA receptors have little or no relevance in the behavioral sensitization produced by 20 mg/kg PCP. In a model using 5 mg/kg PCP, the effects of sulpiride and SCH23390replicated those observed with 20 mg/kg PCP and further showed that acute locomotor activation is not a strict requirement for the development of sensitization. These data argue that there is overlap, but nonidentity, between the mechanisms underlying PCP-induced sensitization and neurotoxicity.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 22/01/20 alle ore 18:30:11