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<p>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 (Glu<sup>V1→LP</sup> 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 Glu<sup>V1→LP</sup> neurons activity was predominantly due to a decrease in the guanine nucleotide-binding protein subunit gamma-4 (Gγ4). Overexpression of Gγ4 in the Glu<sup>V1→LP</sup> 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.</p>

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

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年2月6日

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  • 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,
  • Zhijun Zhang

摘要

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.