Disruption of the anterior commissure in Olig2 deficient mice
Disruption of the anterior commissure in Olig2 deficient mice
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DOI：
10.1111/ejn.15861
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发表时间：
2022-11-23
影响因子：
3.4
通讯作者：
Ono，Katsuhiko
中科院分区：
文献类型：
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作者：
Gotoh，Hitoshi;Maruyama，Kohei;Ono，Katsuhiko
在本研究中，我们检查了Olig 2敲除（Olig 2-KO）小鼠模型前脑中的神经回路形成，并发现胎儿晚期前连合的破坏。前连合的轴突束遇到第三脑室壁，轴突延伸停止。L1-CAM免疫组化显示Olig 2-KO小鼠基底前脑交叉形成缺失。DiI示踪显示，前连合轴突的细束穿过中线，但停止进一步延伸到对侧的深部。此外，DiI标记的轴突的一些部分朝向背外侧，这在对照小鼠前脑中没有观察到。Olig 2-KO小鼠的第三脑室喙部比野生型小鼠宽得多，这可能导致中线融合延迟以及随后的前连合延迟和畸形。我们使用公共数据库分析了Olig 2-KO小鼠的基因表达变化，发现与轴突导向和上皮-间质转化相关的多个基因显示出细微的表达变化。这些结果表明Olig 2可能通过调节多种生物学过程对前连合的形成至关重要。
In the present study, we examined neural circuit formation in the forebrain of theOlig2knockout (Olig2‐KO) mouse model and found disruption of the anterior commissure at the late foetal stage. Axon bundles of the anterior commissure encountered the wall of the third ventricle and ceased axonal extension. L1‐CAM immunohistochemistry showed thatOlig2‐KO mice lose decussation formation in the basal forebrain. DiI tracing revealed that the thin bundles of the anterior commissure axons crossed the midline but ceased further extension into the deep part of the contralateral side. Furthermore, some fractions of DiI‐labelled axons were oriented dorsolaterally, which was not observed in the control mouse forebrain. The rostral part of the third ventricle was much wider in theOlig2‐KO mice than in wild‐type mice, which likely resulted in the delay of midline fusion and subsequent delay and malformation of the anterior commissure. We analysed gene expression alterations in theOlig2‐KO mice using a public database and found multiple genes, which are related to axon guidance and epithelial‐mesenchymal transition, showing subtle expression changes. These results suggest thatOlig2is essential for anterior commissure formation, likely by regulating multiple biological processes.