イシヅカ　ユウタ   Yuta Ishizuka   石塚　佑太    所属   川崎医科大学  医学部 基礎医学　病態代謝学    職種   講師
論文種別	原著
言語種別	英語
査読の有無	査読あり
表題	The anthraquinone derivative emodin attenuates methamphetamine-induced hyperlocomotion and startle response in rats.
掲載誌名	正式名：Pharmacology, biochemistry, and behavior 略　 称：Pharmacol Biochem Behav ISSNコード：18735177/00913057
掲載区分	国外
出版社	ELSEVIER
巻・号・頁	97(2),pp.392-8
著者・共著者	Makoto Mizuno, Hiroki Kawamura, Yuta Ishizuka, Hidekazu Sotoyama, Hiroyuki Nawa
発行年月	2010/12
概要	Abnormal signaling mediated by epidermal growth factor (EGF) or its receptor (ErbB) is implicated in the neuropathology of schizophrenia. Previously, we found that the anthraquinone derivative emodin (3-methyl-1,6,8-trihydroxyanthraquinone) inhibits ErbB1 signaling and ameliorates behavioral deficits of the schizophrenia animal model established by EGF challenge. In the present study, we assessed acute and subchronic effects of its administration on methamphetamine-triggered behavioral hyperactivation in rats. Prior subchronic administration of emodin (50mg/kg/day, 5days, p.o.) suppressed both higher acoustic startle responses and hyperlocomotion induced by acute methamphetamine challenge. In parallel, emodin also attenuated methamphetamine-induced increases in dopamine and its metabolites and decreases in serotonin and its metabolites. Emodin administered alone also had an effect on stereotypic movement but no influence on horizontal or vertical locomotor activity. In contrast to pre-treatment, post-treatment with emodin had no effect on behavioral sensitization to methamphetamine. Administration of emodin in parallel to or following repeated methamphetamine challenge failed to affect hyperlocomotion induced by methamphetamine re-challenges. These findings suggest that emodin has unique pharmacological activity, which interferes with acute methamphetamine signaling and behavior.
DOI	10.1016/j.pbb.2010.09.009
PMID	20863847