A visual cortical-lateral posterior thalamic nucleus circuit regulates depressive-like behaviors in male mice

Fangfang Wu (), Chenxi Gu, Rui Xu, Junwei Ma, Lei Gao, Youjiao Zhang, Siyuan Bu, Qingbo Lu, Te Zhao, Yijun Han, Chen Guo, Yihui Cui, Jianhua Ding, Gang Hu () and Zhijun Zhang ()
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Fangfang Wu: Nanjing University of Chinese Medicine
Chenxi Gu: Nanjing Medical University
Rui Xu: Nanjing University of Chinese Medicine
Junwei Ma: Nanjing University of Chinese Medicine
Lei Gao: Nanjing University of Chinese Medicine
Youjiao Zhang: Nanjing University of Chinese Medicine
Siyuan Bu: Southeast University
Qingbo Lu: Southeast University
Te Zhao: Chinese Academy of Sciences
Yijun Han: Chinese Academy of Sciences
Chen Guo: Zhejiang University School of Medicine
Yihui Cui: Zhejiang University School of Medicine
Jianhua Ding: Nanjing Medical University
Gang Hu: Nanjing University of Chinese Medicine
Zhijun Zhang: Southeast University

Nature Communications, 2025, vol. 16, issue 1, 1-17

Abstract: Abstract Depression, a prevalent psychiatric disorder of ambiguous etiology and high heterogeneity, has been recently linked to the primary visual cortex (V1). However, the precise circuits mediating the impact of V1 on depressive-like behaviors are poorly understood. Here, we demonstrate that the V1, specifically the lateral posterior nucleus of the thalamus (LP)-projecting V1 glutamatergic subpopulation (GluV1→LP neurons), shows reduced activity after chronic restraint stress (CRS) in male mice, leading to depressive-like behaviors. Optogenetic or chemogenetic activation of these neurons ameliorated depressive-like behaviors in CRS-depressed mice, whereas reducing activity exacerbated these behaviors. This reduction in GluV1→LP neurons activity was predominantly due to a decrease in the guanine nucleotide-binding protein subunit gamma-4 (Gγ4). Overexpression of Gγ4 in the GluV1→LP neurons produced antidepressant-like effects, suggesting that Gγ4 is a crucial regulator of mood. Collectively, these results reveal a V1→LP circuit that modulates depressive-like behaviors, suggesting potential targets for therapeutic interventions.

Date: 2025
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DOI: 10.1038/s41467-024-55600-4

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