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Lamotrigine blocks apoptosis induced by repeated administration of high-dose methamphetamine in the medial prefrontal cortex of rats.
| 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)
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Submitter: 仲唐 安哉
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