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Titolo:
Antagonism at 5-HT2A receptors potentiates the effect of haloperidol in a conditioned avoidance response task in rats
Autore:
Wadenberg, MLG; Browning, JL; Young, KA; Hicks, PB;
Indirizzi:
Scott & White Mem Hosp, Temple, TX 76508 USA Scott & White Mem Hosp Temple TX USA 76508 Mem Hosp, Temple, TX 76508 USA Scott & White Clin, Dept Psychiat, Temple, TX 76508 USA Scott & White Clin Temple TX USA 76508 ept Psychiat, Temple, TX 76508 USA Texas A&M Univ, Coll Med, Hlth Sci Ctr, College Stn, TX 77843 USA Texas A&M Univ College Stn TX USA 77843 ci Ctr, College Stn, TX 77843 USA Cent Texas Vet Hlth Care Syst, Neurosci Lab, Waco, TX 76711 USA Cent TexasVet Hlth Care Syst Waco TX USA 76711 i Lab, Waco, TX 76711 USA
Titolo Testata:
PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR
fascicolo: 3, volume: 68, anno: 2001,
pagine: 363 - 370
SICI:
0091-3057(200103)68:3<363:AA5RPT>2.0.ZU;2-D
Fonte:
ISI
Lingua:
ENG
Soggetto:
EMISSION TOMOGRAPHIC ANALYSIS; PREPULSE INHIBITION DEFICITS; ATYPICAL ANTIPSYCHOTIC-DRUGS; DOPAMINE D-2 RECEPTORS; INDUCED CATALEPSY; PREFRONTAL CORTEX; NEGATIVE SYMPTOMS; NEUROLEPTIC DRUGS; NUCLEUS-ACCUMBENS; H-3 MDL-100,907;
Keywords:
sirotonin-2A receptor; dopamine D-2 receptor; conditioned avoidance response behavior; catalepsy; atypical antipsychotic drugs; rat;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
63
Recensione:
Indirizzi per estratti:
Indirizzo: Wadenberg, MLG Karolinska Inst, Dept Physiol & Pharmacol, SE-17177 Stockholm, Sweden Karolinska Inst Stockholm Sweden SE-17177 ockholm, Sweden
Citazione:
M.L.G. Wadenberg et al., "Antagonism at 5-HT2A receptors potentiates the effect of haloperidol in a conditioned avoidance response task in rats", PHARM BIO B, 68(3), 2001, pp. 363-370

Abstract

High affinity for serotonin-2A (5-HT2A) over dopamine (DA) D-2 receptors is a leading hypothesis for clozapine's favorable therapeutic profile. Recent preclinical studies also indicate that a sufficient antipsychotic effect might be obtained by a combined high 5-HT2A/low D2 receptor blockade. Thus,addition of a 5-HT2A receptor antagonist to an ineffective dose of a D-2 receptor antagonist produces a robust antipsychotic-like effect in the conditioned avoidance response (CAR) test. Electrophysiological and biochemical studies also show that 5-HT2A receptor antagonists can confer an atypical (clozapine-like) profile an a D-2 receptor antagonist. Improved therapeutic efficacy by adjunctive 5-HT2A receptor antagonist treatment to a traditional D-2 receptor blocking regimen has been suggested. However, the ability of5-HT2A receptor blockade to protect against, or ameliorate, parkinsonian symptoms still remains unclear. Using the CAR and the catalepsy (CAT) tests as indices for antipsychotic activity and extrapyramidal side effect (EPS) liability, respectively, the effects of the selective 5-HT2A receptor antagonist MDL 100,907 in combination with the DA D-2 receptor antagonists haloperidol or raclopride were studied in rats. Haloperidol (0.025 or 0.1 mg/kg sc, -30 min) produced a dose-dependent suppression of CAR. Pretreatment with MDL 100,907 (0.5, 1.0, or 1.5 mg/kg sc, - 60 min) enhanced and prolonged the haloperidol-induced suppression of CAR without escape failures. MDL 100,907 (1 mg/kg sc, - 60 min) had no effect on CAT when coadministered with ineffective doses of raclopride. Raclopride (1 mg/kg sc, - 30 min) alone produced a submaximal cataleptic response that was significantly enhanced by pretreatment with MDL 100,907. The present results confirm and extend previous results by showing that 5-HT2A receptor blockade can enhance the antipsychotic-like effects of a very low dose of a commonly used traditional antipsychotic. 5-HT2A receptor blockade does not, however, prevent EPS (CAT). The therapeutic advantage of this combination might, therefore, operate within a fairly narrow window. (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 27/01/20 alle ore 15:14:59