Treatment of the Psychostimulant-Sensitized Animal Model of Schizophrenia

被引：16

作者：

Shuto, Takahide ^{[1
]}

Nishi, Akinori ^{[1
]}

机构：

[1] Kurume Univ, Sch Med, Dept Pharmacol, Fukuoka 8300011, Japan

来源：

CNS NEUROSCIENCE & THERAPEUTICS | 2011年 / 17卷 / 02期

基金：

日本学术振兴会;

关键词：

Behavioral sensitization; Dopamine; Schizophrenia; INDUCED BEHAVIORAL SENSITIZATION; 5-HT3 RECEPTOR ANTAGONIST; MEDIAL PREFRONTAL CORTEX; MIDBRAIN DOPAMINE NEURONS; VENTRAL TEGMENTAL AREA; LONG-TERM POTENTIATION; MEDIUM SPINY NEURONS; COCAINE SENSITIZATION; NUCLEUS-ACCUMBENS; SYNAPTIC PLASTICITY;

D O I：

10.1111/j.1755-5949.2010.00218.x

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

P>Behavioral sensitization to psychostimulants in rodents is associated with the alteration of dopaminergic neurotransmission, and has been proposed as a useful model of schizophrenia due to its progressively intensifying, easily relapsing, and long-lasting features. Pharmacological treatments that reverse the established sensitization may have potential therapeutic values for schizophrenia. The present aim is to review pharmacological treatments that induce the reversal of established sensitization to psychostimulants. In addition, we discuss possible mechanisms for the reversal of sensitization. Reversal of sensitization is induced by chronic dopamine D1 receptor agonism, D2 or D1/D2 receptor agonism combined with mild N-methyl-D-aspartate (NMDA) receptor antagonism or serotonin (5-HT(2A) or 5-HT(3)) receptor antagonism, 5-HT(1A) receptor agonism, and 5-HT(2A) or 5-HT(3) receptor antagonism. Chronic treatments with these drugs likely adjust altered dopaminergic neurotransmission in sensitized animals. Especially, chronic dopamine D1 receptor agonism, which may adjust mesolimbic hyperdopaminergic and mesocortical hypodopaminergic functions in sensitized animals, is an attractive therapeutic approach for schizophrenia.

引用

页码：133 / 139

页数：7

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