南京医科大学肖明小组的论文发现了少突胶质细胞Egr2介导再社会化对社会孤立小鼠社会能力的有益影响。2025年11月6日出版的《神经科学通报》发表了这项成果。

早期社会孤立会损害社会能力，这种能力在重新社会化后可以部分恢复，但其潜在机制很少得到解决。该研究报道，青春期SI小鼠与GH小鼠重新社交，而不是与SI小鼠重新社交，表现出改善的社交行为表现，内侧前额叶皮层（mPFC）髓鞘形成增加，少突胶质细胞（OLs）中Egr2表达上调。在生长激素同伴中特异性下调OL Egr2或在SI同伴中过度表达OL Egr2，分别消除或恢复了它们对SI小鼠mPFC低髓鞘化和社交能力缺陷的修复作用。

此外，生长激素对SI小鼠mPFC中OL Egr2表达和髓鞘形成的改善作用在皮质酮作用下被消除RNA测序分析显示，Egr2通过抑制PDGFRα增强髓鞘形成。总之，这些结果表明，Egr2/PDGFRα轴在挽救SI诱导的髓鞘退化和社交能力障碍中介导了明显的同伴效应。

附：英文原文

Title: Oligodendrocyte Egr2 Mediates the Beneficial Effect of Resocialization on the Social Ability of Socially Isolated Mice

Author: Zhang, Yanli, Chen, Sijia, Zhang, Shuying, Li, Yue, Wang, Yimiao, Cao, Min, Jin, Yuxi, Wang, Ze, Ding, Shixin, Xiao, Ming

Issue&Volume: 2025-11-06

Abstract: Early social isolation (SI) impairs social ability, which can be partially rescued after resocialization, but the underlying mechanisms have been rarely addressed. This study reported that adolescent SI mice resocialized with group housing (GH) mice, but not with SI mice, showed improved social behavior performances, increased myelination in the medial prefrontal cortex (mPFC), and upregulated Egr2 expression in oligodendrocytes (OLs). Specific down-regulation of OL Egr2 in GH companions or overexpression of OL Egr2 in SI peers abolished or rescued their repair effects on mPFC hypomyelination and social ability defects in SI mice, respectively. Furthermore, the improving effect of GH companions on OL Egr2 expression and myelinogenesis in the mPFC of SI mice was abolished when GH mice were treated with corticosterone. RNA-sequencing analysis showed that Egr2 enhanced myelination by inhibiting PDGFRα. Together, these results revealed that the Egr2/PDGFRα axis mediates distinct peer effects in rescuing SI-induced hypomyelination and social ability impairment.

DOI: 10.1007/s12264-025-01534-w

Source: https://link.springer.com/article/10.1007/s12264-025-01534-w