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2015年09月15日

Early life experience change dendrite patterning and neuronal connectivity

日 時 2015年09月15日(火) 16:00 より 17:00 まで
講演者 下郡智美博士
講演者所属 理研BSI
場 所 生理研(明大寺) 1階 セミナー室
お問い合わせ先 視覚情報処理研究部門、吉村由美子 yumikoy@nips.ac.jp
要旨

理研BSIの下郡智美博士にセミナーをお願いしました。このセミナーは英語で行われます。多数のご参集をお待ちしています。

There are many evidences that experience changes neuronal circuit to make stronger connection or remove unnecessary connection to avoid mis-wiring. However, how exactly neuronal activity refines neuronal circuit is largely unknown.  I will introduce our recent findings, which is about detailed molecular mechanism of neuronal input dependent dendrite patterning in mammalian cerebral cortex.   In our previous study, we showed BTB domain containing protein (BTBD3) plays important role to change dendrite orientation toward higher neuronal input.  We also showed that function of BTBD3 is conserved in mouse somatosensory cortex and ferret visual cortex.  We have further revealed partner molecule for BTBD3 to respond to neuronal activity and remove excess dendrite.  Knock out mouse of BTBD3 partner molecule showed aberrant dendrite pruning activity.  Lack of BTBD3 biding domain also showed altered dendrite pruning activity in mouse somatosensory cortex.  Finally we revealed that the molecular pathway is conserved in ferret visual cortex to control visual input dependent dendrite patterning in ocular dominance column.   Taken together, the results implicate discrete molecular mechanisms for high-resolution sensory function.