Neurotrophin-3 influences the number and the laminar fate of cortical progenitors in the developing cerebral cortex of mice through the MEK/ERK1/2 signaling pathway.

Neurotrophin-3 influences the number and the laminar fate of cortical progenitors in the developing cerebral cortex of mice through the MEK/ERK1/2 signaling pathway.
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DOI:
10.2220/biomedres.34.231
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发表时间:
2013
期刊:
Biomedical research
影响因子:
--
通讯作者:
Masanari Ohtsuka;Hitomi Soumiya;M. Hanai;S. Furukawa;H. Fukumitsu
Masanari Ohtsuka;Hitomi Soumiya;M. Hanai;S. Furukawa;H. Fukumitsu
中科院分区:
其他
文献类型:
--
作者:
Masanari Ohtsuka;Hitomi Soumiya;M. Hanai;S. Furukawa;H. Fukumitsu

文献摘要

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发育中的大脑皮层中的层状形成需要精确调节表型特异性神经元的产生。为了确定是否神经营养因子-3(NT 3)参与这种形成,我们研究了NT 3在端脑脑室空间给药对13.5日龄小鼠胚胎的影响。NT 3增加了新产生的神经元的数量,并改变了神经元的表型的位置和转录因子的表达谱;原来致力于第IV层神经元的神经元表型被改变为第II/III层神经元。当亲本祖细胞在G1期至S期暴露于NT 3时观察到前一种效应,而在G1期暴露时观察到后一种效应。此外,在体外实验中发现,在分离的原代培养的皮质祖细胞中观察到NT 3的层状命运改变,并且NT 3的作用被MEK/ERK抑制剂共同处理所抑制。这些观察结果表明,NT 3是通过细胞间MEK/ERK途径参与层状形成的发育中的大脑皮层。
The laminar formation in the developing cerebral cortex requires precisely regulated generation of phenotype-specific neurons. To determine whether neurotrophin-3 (NT3) is involved in this formation, we investigated the effects of NT3 administration in the telencephalic ventricular space on 13.5-day-old mouse embryos. NT3 increased the number of newly generated neurons and altered the neuronal phenotypes in the position and the transcription factors-expression profiles; the neuronal phenotypes originally committed for layer IV neurons were altered toward for layers II/III neurons. The former effects were observed when the parent progenitor cells were exposed to NT3 in the G1- to S-phase, whereas the latter effects were observed with exposure in the G1-phase. In addition, in vitro experiments revealed that the laminar fate alteration by NT3 was observed in the dissociated primary culture of cortical progenitors and the NT3 actions were suppressed by cotreatment with the MEK/ERK inhibitor. These observations suggest that NT3 is involved in the laminar formation of the developing cerebral cortex through the intercellular MEK/ERK pathway.