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

Molecular Psychiatry (2025)Cite this article

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Abstract

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.

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Fig. 1: The decreased neuronal firing of dDG is intimately associated with chronic stress induced social avoidance and social recognition impairment.
Fig. 2: Chronic stress impairs the neural excitability of the dDG and vDG probably due to the dysfunction of NALCN.
Fig. 3: NALCN in the dDG neurons is a molecular target of chronic stress induced social avoidance and social recognition impairment.
Fig. 4: NALCN reduction in the dDG glutamatergic neurons specifically reproduces social avoidance and social recognition impairment.
Fig. 5: NALCN reduction in the dDG glutamatergic neurons decreases neural excitability and lowers neurons firing during social interactions.
Fig. 6: Increasing NALCN expression in the dDG glutamatergic neurons alleviates chronic stress-induced social deficits through enhancing neuronal excitability.
Fig. 7: Activation of the dDG–MS glutamatergic projection rescues chronic stress-induced social deficits.

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Data availability

The data that support the findings of this study are presented in the form of graphs and available from the corresponding author upon reasonable request.

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Acknowledgements

This study is supported by the National Natural Science Foundation of China [Grant No. 82301360, to JPW] and [Grant No. 82271290, to CZ] and [Grant No. 82371281, to TZ]; Natural Science Foundation of Sichuan Province [Grant No. 2023NSFSC1488, to JPW] and [Grant No. 2023ZYD0168, to CZ].

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  1. These authors contributed equally: Jinping Wang, Lanyu Zhang.

Authors and Affiliations

  1. Department of Anesthesiology, West China Hospital, Sichuan University, Chengdu, 610041, China

    Jinping Wang, Lanyu Zhang, Jin Liu, Yaoxin Yang, Yusi Hua, Tao Zhu & Guo Chen

  2. Research Center of Anesthesiology, National-Local Joint Engineering Research Centre of Translational Medicine of Anesthesiology, West China Hospital, Sichuan University, Chengdu, 610041, China

    Jinping Wang & Cheng Zhou

  3. Department of Anesthesiology, West China Second University Hospital, Sichuan University, Chengdu, 610041, China

    Xinchuan Wei & Xiaoqin Jiang

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Contributions

CZ, GC and JL designed the research. JW YZ and YY performed the research including virus injection, behavioral tests, and electrophysiological recordings. XW, and TZ analyzed the data. XJ and YH prepared figures and created illustrations. JW, and CZ wrote the manuscript. All authors read and approved the final manuscript.

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Correspondence to Guo Chen or Cheng Zhou.

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Wang, J., Zhang, L., Liu, J. et al. Stress-induced reduction of sodium leak currents causes social deficits by impairing dorsal dentate gyrus-medial septum glutamatergic projection. Mol Psychiatry (2025). https://doi.org/10.1038/s41380-025-03101-1

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