The antipsychotic-like effects of clozapine in C57BL/6 mice exposed to cuprizone: Decreased glial activation

Cuprizone (CPZ), a copper chelator that has been shown to selectively damage white matter, can induce a novel animal model to mimic some symptoms of schizophrenia. This study aimed to examine the effect of clozapine (CLZ) on behavioural changes induced by CPZ exposure and try to explore the underlyi...

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Bibliographic Details
Published in:Behavioural brain research 2019-05, Vol.364, p.157-161
Main Authors: Chang, HaoXiao, Wei, YuZhen, Chen, YuJing, Du, Li, Cong, HengRi, Zhang, XingHu, Geng, XingChao, Yin, LinLin
Format: Article
Language:English
Subjects:
Animals
Antipsychotic Agents - pharmacology
Behavior, Animal - drug effects
Behaviour abnormality
Clozapine
Clozapine - pharmacology
Cuprizone
Cuprizone - pharmacology
Disease Models, Animal
Glial activation
Male
Mice
Mice, Inbred C57BL
Neuroglia - drug effects
Schizophrenia
Schizophrenia - chemically induced
Schizophrenia - metabolism
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Summary:Cuprizone (CPZ), a copper chelator that has been shown to selectively damage white matter, can induce a novel animal model to mimic some symptoms of schizophrenia. This study aimed to examine the effect of clozapine (CLZ) on behavioural changes induced by CPZ exposure and try to explore the underlying mechanisms. Behavioural abnormalities associated with feeding mice a 0.4% (w/w) CPZ-containing diet were assessed by Y-maze, spontaneous locomotor activity, and climbing tests. CLZ treatment reversed the increase in total explored distance, exploring velocity, locomotor movements, climbing behaviours and glial activation induced by CPZ exposure. Our findings indicate that increased glial activation may be related to behavioural abnormalities in CPZ exposure mice and that anti-inflammatory properties may be involved in the CLZ mechanisms. CPZ short-term exposure with a higher dosage may offer a useful model to study some aspects of schizophrenia and evaluate the efficacy of antipsychotics.
ISSN:0166-4328
1872-7549
DOI:10.1016/j.bbr.2019.02.026