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Integrative function of higher-order behaviors through interaction of brain neural circuitry

開催日 2014/9/11
時間 17:00 - 19:00
会場 Room B(501)
Chairperson(s) 喜田 聡 / Satoshi Kida (東京農業大学 応用生物科学部バイオサイエンス学科 / Department of Bioscience, Tokyo University of Agriculture, Japan)
小林 和人 / Kazuto Kobayashi (福島県立医科大学 医学部 生体機能研究部門 / Department of Molecular Genetics, Fukushima Medical University, Japan)

Corticostriatal circuits mediating learning

  • S1-B-3-1
  • Andrew Holmes:1 
  • 1:NIH, USA 

Prior studies have found compelling evidence of alterations in cognition and emotional regulation following acute or repeated alcohol exposure but have not established the mechanisms involved. This presentation will discuss studies testing whether chronic intermittent alcohol exposure (CIE), via vapor inhalation, in C57BL/6J mice impaired fear extinction and produced associated functional adaptations in dorsal striatum and medial prefrontal cortex (mPFC). Results will be shown demonstrating that CIE impaired extinction and facilitated rewarded learning and did so in the absence of alterations in fear, anxiety or tolerance, at least on the tests employed. These behavioral deficits were associated with dendritic remodeling of pyramidal neurons in the prelimbic cortex subregion of mPFC (but not infralimbic cortex or orbitofrontal cortex (OFC). To further examine for functional changes in mPFC and striatal neurons after CIE, in vivo neuronal recordings from multichannel electrodes were conducted as mice underwent extinction. Results will be shown that are consistent with abnormal neuronal encoding of behavior, including reduced neuronal burst firing occurred in mPFC neurons. Finally, recent work will be shown that uses optogenetic techniques to define the mPFC and striatal circuits mediating rewarded learning and fear extinction. Collectively, this presentation will propose a model in which CIE modifies behavior by producing structural and functional alterations in mPFC neurons. These findings could have implications for understanding the mechanistic basis for the co-occurrence of alcoholism and certain anxiety disorders.

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