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<p>The neural basis of anxiety is unclear, which hinders the treatment of anxiety disorders. Here, we found that αCaMKII<sup>+</sup> neurons in the medial prefrontal cortex (mPFC<sup>αCaMKII+</sup>) responded to stressors with increased activity both under physiological conditions and after repeated restraint stress (RRS) in mice. Chemogenetic activation of mPFC<sup>αCaMKII+</sup> neurons ameliorated stress-induced anxiety. A delayed increase in the expression of growth hormone secretagogue receptor 1a (GHS-R1a), the receptor of the peripheral metabolic hormone ghrelin, in mPFC<sup>αCaMKII+</sup> neurons coincided with reduced excitatory synaptic transmission and the development of RRS-induced enhancement of anxiety-related behavior. Virus-mediated GHS-R1a upregulation in mPFC<sup>αCaMKII+</sup> neurons exaggerated the excitation/inhibition (E/I) imbalance and promoted anxiety-related behavior, whereas GHS-R1a knockdown had the opposite effect. We conclude that GHS-R1a signaling contributes to the development of stress-induced anxiety by shaping synaptic activity of mPFC<sup>αCaMKII+</sup> neurons. GHS-R1a may be a new therapeutic target for treating anxiety disorders.</p>

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Stress-induced GHS-R1a expression in medial prefrontal cortical neurons promotes vulnerability to anxiety in mice

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年3月13日

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  • Liu Yang,
  • Meng Zhang,
  • Xiaomin Sun,
  • Anqi Du,
  • Jiajia Jia,
  • Nan Li,
  • Gonghui Hu,
  • Yingchang Lu,
  • Sihan Wang,
  • Jingsai Zhang,
  • Wenjie Chen,
  • Hanbing Yu,
  • Yu Zhou

摘要

The neural basis of anxiety is unclear, which hinders the treatment of anxiety disorders. Here, we found that αCaMKII+ neurons in the medial prefrontal cortex (mPFCαCaMKII+) responded to stressors with increased activity both under physiological conditions and after repeated restraint stress (RRS) in mice. Chemogenetic activation of mPFCαCaMKII+ neurons ameliorated stress-induced anxiety. A delayed increase in the expression of growth hormone secretagogue receptor 1a (GHS-R1a), the receptor of the peripheral metabolic hormone ghrelin, in mPFCαCaMKII+ neurons coincided with reduced excitatory synaptic transmission and the development of RRS-induced enhancement of anxiety-related behavior. Virus-mediated GHS-R1a upregulation in mPFCαCaMKII+ neurons exaggerated the excitation/inhibition (E/I) imbalance and promoted anxiety-related behavior, whereas GHS-R1a knockdown had the opposite effect. We conclude that GHS-R1a signaling contributes to the development of stress-induced anxiety by shaping synaptic activity of mPFCαCaMKII+ neurons. GHS-R1a may be a new therapeutic target for treating anxiety disorders.