Scholarlink

<p>Stress-induced social deficits are related with the malfunction of dentate gyrus (DG). However, the exact molecular mechanism and/or neural circuit of DG participated in social impairments induced by chronic stress is not fully known. Here, we report that the sodium leak channel (NALCN) reduction in the dorsal DG (dDG) but not the ventral DG (vDG) induces social deficits of chronic stress through lowering the excitability and the firings of the glutamatergic neurons. Furthermore, the present study reveals that the medial septum (MS) is an important downstream projection region of dDG glutamatergic neurons involved in the social impairments of chronic stress; and activating the dDG-MS glutamatergic projection significantly relieves these social deficits. In summary, these findings indicate that NALCN in dDG glutamatergic neurons presents a promising molecular target for social deficits of chronic stress <i>via</i> influencing the activity of the dDG glutamatergic neurons (dDG<sup>Glu</sup>) and their projection to the MS.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Stress-induced reduction of sodium leak currents causes social deficits by impairing dorsal dentate gyrus-medial septum glutamatergic projection

  • 期刊论文

  • 发表日期：

    2025年7月2日

查看全文
  • Jinping Wang,
  • Lanyu Zhang,
  • Jin Liu,
  • Yaoxin Yang,
  • Xinchuan Wei,
  • Xiaoqin Jiang,
  • Yusi Hua,
  • Tao Zhu,
  • Guo Chen,
  • Cheng Zhou

摘要

Stress-induced social deficits are related with the malfunction of dentate gyrus (DG). However, the exact molecular mechanism and/or neural circuit of DG participated in social impairments induced by chronic stress is not fully known. Here, we report that the sodium leak channel (NALCN) reduction in the dorsal DG (dDG) but not the ventral DG (vDG) induces social deficits of chronic stress through lowering the excitability and the firings of the glutamatergic neurons. Furthermore, the present study reveals that the medial septum (MS) is an important downstream projection region of dDG glutamatergic neurons involved in the social impairments of chronic stress; and activating the dDG-MS glutamatergic projection significantly relieves these social deficits. In summary, these findings indicate that NALCN in dDG glutamatergic neurons presents a promising molecular target for social deficits of chronic stress via influencing the activity of the dDG glutamatergic neurons (dDGGlu) and their projection to the MS.