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锌指基因Fezf2是杏仁核基底外侧复合体中兴奋性神经元发育所必需的。

The zinc finger gene Fezf2 is required for the development of excitatory neurons in the basolateral complex of the amygdala.

作者信息

Hirata-Fukae Chiho, Hirata Tsutomu

机构信息

Senior Research Fellow Center, Ehime University, Ehime, Japan.

出版信息

Dev Dyn. 2014 Aug;243(8):1030-6. doi: 10.1002/dvdy.24137. Epub 2014 May 2.

DOI:10.1002/dvdy.24137
PMID:24723342
Abstract

BACKGROUND

The basolateral complex, comprised of the lateral, basolateral, and basomedial nuclei, is the main structure of the amygdala and contains two neuronal cell types: excitatory neurons and inhibitory interneurons. Studies show that most of the excitatory neurons originate in the ventral pallium of the telencephalon. However, their subsequent development remains poorly understood.

RESULTS

In this study, we examined the roles of the zinc finger gene Fezf2 in the development of the amygdala. Fezf2 is expressed in the lateral and basolateral nuclei during development. In Fezf2-deficient embryos, specific excitatory neuron markers in the lateral and basolateral nuclei were reduced, with concurrent induction of other markers in the endopiriform cortex. Furthermore, the morphology of the lateral and basolateral nuclei was abnormal. In the adult stages, excitatory neurons in the lateral and basolateral nuclei were greatly reduced because of apoptosis that occurred soon after birth.

CONCLUSIONS

These results suggest that Fezf2 is required for the development of excitatory neurons and nuclear morphology in the lateral and basolateral nuclei, and that abnormal formation of these regions leads to cell death soon after birth in Fezf2-deficient mice.

摘要

背景

基底外侧复合体由外侧核、基底外侧核和基底内侧核组成,是杏仁核的主要结构,包含两种神经元细胞类型:兴奋性神经元和抑制性中间神经元。研究表明,大多数兴奋性神经元起源于端脑的腹侧 pallium。然而,它们随后的发育仍知之甚少。

结果

在本研究中,我们研究了锌指基因 Fezf2 在杏仁核发育中的作用。Fezf2 在发育过程中在外侧核和基底外侧核中表达。在 Fezf2 缺陷胚胎中,外侧核和基底外侧核中的特定兴奋性神经元标记物减少,同时在内梨状皮质中诱导其他标记物。此外,外侧核和基底外侧核的形态异常。在成年阶段,外侧核和基底外侧核中的兴奋性神经元由于出生后不久发生的凋亡而大大减少。

结论

这些结果表明,Fezf2 是外侧核和基底外侧核中兴奋性神经元发育和核形态所必需的,并且这些区域的异常形成导致 Fezf2 缺陷小鼠出生后不久细胞死亡。

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