オシブチ ヒデヒロ   OSHIBUCHI Hidehiro
  押淵 英弘
   所属   医学部 医学科(東京女子医科大学病院)
   職種   准教授
論文種別 総説
言語種別 日本語
査読の有無 査読なし
表題 [Significance of the pharmacotherapy of schizophrenia in the emotional context processing of cognition].
掲載誌名 正式名:Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology
略  称:Nihon Shinkei Seishin Yakurigaku Zasshi
ISSNコード:(1340-2544)1340-2544(Linking)
掲載区分国内
巻・号・頁 33(3),101-104頁
著者・共著者 Inada Ken, Oshibuchi Hidehiro, Shigooka Jun
発行年月 2013/06
概要 Emotional disorders and cognitive dysfunctions are important treatment targets in psychiatric clinical settings. The biological mechanisms of emotional disorders have been studied with methods that include fear conditioning, schizophrenia models are studied with methamphetamine-induced reverse tolerance in rats, and dynamic changes in brain neurotransmitters are studied with microdialysis and high-performance liquid chromatography. We combined these methods in order to evaluate dopamine dynamics in the amygdala and the biological bases and relationships of emotional disorder and cognitive dysfunction. Fear-conditioned rats showed freezing behavior and dopamine release in the amygdala in response to conditioned stimuli. Methamphetamine-induced reverse tolerance rats showed increased dopamine release in the amygdala in response to conditioned stimuli. The increased release of dopamine continued after the freezing behavior had ended. This increased and long-lasting dopamine release may reflect abnormal emotional context processing in cognition in schizophrenia. Antipsychotic drugs, such as haloperidol, aripiprazole, and clozapine, suppress this increased release of dopamine in the amygdala in response to conditioned stimuli. These findings suggest that antipsychotic drugs may stabilize abnormal emotional context processing in cognition in this model. We conclude that the significance of pharmacotherapy in schizophrenia is that antipsychotic drugs stabilize the emotional context processing in cognition and adjust the relationship of emotion and cognition.
PMID 25069242