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Lamotrigine blocks apoptosis induced by repeated administration of high-dose methamphetamine in the medial prefrontal cortex of rats.

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Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/47184

Title: Lamotrigine blocks apoptosis induced by repeated administration of high-dose methamphetamine in the medial prefrontal cortex of rats.
Authors: Nakato, Yasuya Browse this author
Abekawa, Tomohiro Browse this author
Ito, Koki Browse this author
Inoue, Takeshi Browse this author
Koyama, Tsukasa Browse this author
Keywords: Apoptosis
Lamotrigine
Methamphetamine
Glutamate
Schizophrenia
Issue Date: 3-Mar-2011
Journal Title: Neuroscience letters
Volume: 490
Issue: 3
Start Page: 161
End Page: 164
Publisher DOI: 10.1016/j.neulet.2010.11.028
PMID: 21093543
Abstract: Lamotrigine (LTG) is sometimes co-administered with antipsychotic drugs for the treatment of schizophrenia. Nevertheless, the pharmacological basis of LTG use for schizophrenia has not been reported. Our group recently proposed a new psychostimulant animal model that might reflect the progressive pathophysiology of schizophrenia. Results obtained using that model show that LTG blocks the initiation and expression of repeated high-dosage methamphetamine-induced prepulse inhibition deficit in rats (Nakato et al., 2010, Neurosci. Lett. [25]). Using the model, the effect of LTG (30 mg/kg) on methamphetamine (METH, 2.5 mg/kg)-induced increases in extracellular glutamate levels in the medial prefrontal cortex (mPFC) was examined in this study. Then the effect of repeated co-administration of LTG (30 mg/kg) on repeated METH (2.5 mg/kg)-induced apoptosis in this region of rats was investigated. Results show that LTG (30 mg/kg) blocked the METH (2.5 mg/kg)-induced glutamate increase in the mPFC. Repeated co-administration of LTG (30 mg/kg) blocked the development of apoptosis induced by repeated administration of METH (2.5 mg/kg) in the mPFC. The LTG blocks histological abnormalities induced by repeated administration of METH, which suggests a mechanism of LTG that protects against progressive pathophysiology in schizophrenia.
Type: article (author version)
URI: http://hdl.handle.net/2115/47184
Appears in Collections:医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 仲唐 安哉

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