Phencyclidine-induced cognitive deficits in mice are improved by subsequent subchronic administration of clozapine, but not haloperidol

被引:125
作者
Hashimoto, K
Fujita, Y
Shimizu, E
Iyo, M
机构
[1] Chiba Univ, Ctr Forens Mental Hlth, Div Clin Neurosci, Chiba 2608670, Japan
[2] Chiba Univ, Grad Sch Med, Dept Psychiat, Chiba 2608670, Japan
关键词
schizophrenia; NMDA receptor; phencyclidine; cognition; clozapine; haloperidol;
D O I
10.1016/j.ejphar.2005.07.002
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
This study was undertaken to examine the effects of subsequent administration of antipsychotic drugs (clozapine and haloperidol) on cognitive deficits in mice after repeated administration of phencyclidine (PCP). In the novel object recognition test, repeated administration of PCP (10 mg/kg) significantly decreased exploratory preference in the retention test session but not in the training test session. PCP-induced deficits were significantly improved by subsequent subchronic (2 weeks) administration of clozapine (5 mg/kg), but not haloperidol (0.1 mg/kg). These findings suggest that PCP-induced cognitive deficits using the novel object recognition test may be a potential animal model of atypical antipsychotic activity. (c) 2005 Elsevier B.V. All rights reserved.
引用
收藏
页码:114 / 117
页数:4
相关论文
共 17 条
[1]   The glutamatergic dysfunction hypothesis for schizophrenia [J].
Coyle, JT .
HARVARD REVIEW OF PSYCHIATRY, 1996, 3 (05) :241-253
[2]   Schizophrenia [J].
Freedman, R .
NEW ENGLAND JOURNAL OF MEDICINE, 2003, 349 (18) :1738-1749
[3]   Approaching a consensus cognitive battery for clinical trials in schizophrenia: the NIMH-MATRICS conference to select cognitive domains and test criteria [J].
Green, MF ;
Nuechterlein, KH ;
Gold, JM ;
Barch, DM ;
Cohen, J ;
Essock, S ;
Fenton, WS ;
Frese, F ;
Goldberg, TE ;
Heaton, RK ;
Keefe, RSE ;
Kern, RS ;
Kraemer, H ;
Stover, E ;
Weinberger, DR ;
Zalcman, S ;
Marder, SR .
BIOLOGICAL PSYCHIATRY, 2004, 56 (05) :301-307
[4]   Decreased serum levels of D-serine in patients with schizophrenia - Evidence in support of the N-methyl-D-aspartate receptor hypofunction hypothesis of schizophrenia [J].
Hashimoto, K ;
Fukushima, T ;
Shimizu, E ;
Komatsu, N ;
Watanabe, H ;
Shinoda, N ;
Nakazato, M ;
Kumakiri, C ;
Okada, S ;
Hasegawa, H ;
Imai, K ;
Iyo, M .
ARCHIVES OF GENERAL PSYCHIATRY, 2003, 60 (06) :572-576
[5]   Dysfunction of Glia-Neuron Communication in Pathophysiology of Schizophrenia [J].
Hashimoto, Kenji ;
Shimizu, Eiji ;
Iyo, Masaomi .
CURRENT PSYCHIATRY REVIEWS, 2005, 1 (02) :151-163
[6]  
Hashimoto Kenji, 2004, Current Medicinal Chemistry - Central Nervous System Agents, V4, P147, DOI 10.2174/1568015043357011
[7]  
JAVITT DC, 1991, AM J PSYCHIAT, V148, P1301
[8]   The neuropsychopharmacology of phencyclidine: From NMDA receptor hypofunction to the dopamine hypothesis of schizophrenia [J].
Jentsch, JD ;
Roth, RH .
NEUROPSYCHOPHARMACOLOGY, 1999, 20 (03) :201-225
[9]   NMDA agonists and antagonists as probes of glutamatergic dysfunction and pharmacotherapies in neuropsychiatric disorders [J].
Krystal, JH ;
D'Souza, DC ;
Petrakis, IL ;
Belger, A ;
Berman, RM ;
Charney, DS ;
Abi-Saab, W ;
Madonick, S .
HARVARD REVIEW OF PSYCHIATRY, 1999, 7 (03) :125-143
[10]   Repeated administration of phencyclidine, amphetamine and MK-801 selectively impairs spatial learning in mice: a possible model of psychotomimetic drug-induced cognitive deficits [J].
Mandillo, S ;
Rinaldi, A ;
Oliverio, A ;
Mele, A .
BEHAVIOURAL PHARMACOLOGY, 2003, 14 (07) :533-544