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               腦功能基因組學教育部重點實驗室
              Key Laboratory of Brain Functional Genomics, Ministry of Education

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              "Normal and abnormal inductions of synaptic plasticity in rodent prefrontal cortex: possible roles in executive cognitive function"-Satoru Otani

              發布日期: 2016-08-30  瀏覽次數: 45  作者:

              "Normal and abnormal inductions of synaptic plasticity in rodent prefrontal cortex: possible roles in executive cognitive function"-Satoru Otani(University of Pierre and Marie Curie–Paris 6)

              時間: 2010年6月11日10:00-11:30

              地點:理科大樓A-510

              報告題目:Normal and abnormal inductions of synaptic plasticity in rodent prefrontal cortex: possible roles in executive cognitive function

              報告人:大谷悟 博士 University of Pierre and Marie Curie–Paris 6

               

              報告人簡介:神經的可塑性,包括其在神經生理學,神經化學以及認知及行為學等不同領域中的作用。目前的研究主要關注大腦學習和記憶功能的突觸模型:長時程增強()及長時程減弱。以對認知和學習記憶最為關鍵的腦區前額葉及海馬為研究對象,利用電生理及化學藥理學等方法,探討了許多蛋白及分子,如氨基酸受體,胞質鈣離子,胞內第二信使及多種蛋白合成酶對突觸可塑性的影響。現期主要對大小鼠大腦前額葉的突觸可塑性及兒茶酚安,如多巴胺,去甲腎上腺素等對其的調控,進行在體及離體的電生理研究,同時配合相關的行為學及生物化學檢測。

               

              報告簡介:It is increasingly clear that dysregulation of neuroplasticity in the prefrontal cortex (PFC) may underlie cognitive abnormalities seen in certain psychiatric disorders such as schizophrenia and drug addiction. Using rodent in vitro and in vivo model systems, we have been studying synaptic plasticity in the PFC, i.e. long-term potentiation (LTP) and long-term depression (LTD), under various experimental conditions to gain insights into functional and dysfunctional neuroplasticity regulations in the PFC and their possible involvement in executive cognitive function. In this seminar, I will first show how the fast phasic and background tonic dopamine signals regulate normal and abnormal inductions of synaptic plasticity in rat PFC, and propose a mechanistic basis for pathogenesis of schizophrenia cognitive symptom. I will then present our more recent data on the regulatory role of dopamine transporters in synaptic plasticity in the PFC, which may be involved in behavioral rigidity as seen in drug addiction. Third, I will present our in vivo results in which the hippocampus-PFC monosynaptic connection and PFC-dependent cognition are profoundly modified by acute and chronic injections of non-competitive NMDA receptor antagonist MK801, a leading animal model of schizophrenia. Thus, in this seminar, I will present our cutting-edge knowledge obtained in several different model systems, in order to provide a global and comprehensive idea on the possible relation between normal/abnormal plasticity inductions in the PFC and changes of executive cognitive function.

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