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Oral Sessions

Neuronal Differentiation and Migration


開催日 2015/7/28
時間 16:30 - 17:30
会場 Room 9 (Room 3A, Kobe International Exhibition Hall)
Chairperson(s) 仲嶋一範 / Kazunori Nakajima ( 慶應義塾大学医学部解剖学教室 / Department of Anatomy, Keio University School of Medicine )
深澤 有吾 / Yugo Fukazawa (福井大学医学部 脳形態機能解析 / Division of brain structure and function, Faculty of Medical Science, University of Fukui)
  • 1O09-2-2   Time: 16:45 - 17:00

Wnt7b expressed by neurons born on embryonic day 11.5 of mouse brain is necessary for the normal brain morphogenesis

  • 橋本 光広 / Mitsuhiro Hashimoto:1,2 
  • 1:福島県立医大医神経解剖・発生 / Dept Neuroanat, Fukushima Med Univ, Fukushima, Japan 2:名古屋大院医細胞生物 / Dept Cell Biol, Nagoya Univ, Nagoya, Japan 

Wnt7b is a secreted signaling molecule that is involved in intercellular communication and play an important role in neuronal development. In a mouse brain at embryonic day 18.5 (E18.5), neurons born on E11.5 settle in the subplate of neocortex and form several clusters in the cerebellum. Interestingly, these neurons express Wnt7b. To examine the function of Wnt7b in neurons born on E11.5, we used an adenoviral vector expressing antisense RNAs of Wnt7b to suppress Wnt7b-expression. The adenoviral vector successfully suppressed Wnt7b-expression in vitro and in vivo. Wnt7b-suppression in neurons born on E11.5 caused severe malformation of the adult mouse neocortex and cerebellum. The neocortex was small compared with normal brain, and the parvalbumin-positive neurons were reduced. The cerebellar vermis was partially absent, and there was cystic dilatation of the fourth ventricle. These malformations were similar to a human brain disease of Dandy-Walker malformation. By contrast, when the antisense RNAs of Wnt7b were expressed in neurons born on E12.5, the brain malformation did not occur. The observation indicates that Wnt7b-expression in neurons born on E11.5 is important for normal brain morphogenesis and the Wnt7b-suppression in neurons born on E11.5 contributes to a brain malformation.


研究助成:Research funds : 25430008

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