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<p>The body’s defensive emotional reaction to stress presents as anxiety. Nevertheless, long-term anxious stimuli can cause pathological anxiety disorders together with endocrine system, neural system, and immune system dysfunctions. Thus, researchers should understand the neural processes that govern anxiety during stress to create preventive and care plans. By combining behavioral tests, chemogenetic strategies, c-fos stainings, and whole-cell patch clamp recordings, this study looked into the function of dorsal medial prefrontal cortex (dmPFC) mu opioid receptors (MORs), specifically GABAergic MORs (MOR<sub>GABA</sub>), in anxiety-like behavior brought on by acute restraint stress (ARS). The dmPFC MOR<sub>GABA</sub> is triggered during ARS. This activation reduced the inhibitory synaptic input onto projection neurons that target the basolateral amygdala (BLA) by suppressing the activity of neighboring dmPFC GABAergic interneurons. In turn, mice that showed anxiety-like behavior also had higher neural activity of dmPFC-BLA projection neurons. When combined, these results describe a local, MOR<sub>GABA</sub>-mediated dmPFC pathway that governs acute stress-induced anxiety reactions. These findings could offer a possible logical foundation for dmPFC-focused medication screening and anxiety treatment.</p>

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Contributions of dorsal medial prefrontal cortex GABAergic mu opioid receptors on acute restraint stress-induced anxiety-like behavior

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月16日

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  • Yinan Du,
  • Fenghua Xu,
  • Junmin Zhang,
  • Yukui Zhao,
  • Shuyi Liu,
  • Yuan Chang,
  • Yiwei Liu,
  • Yingchun Yang,
  • Yingying Li,
  • Hongyu Qin,
  • Chunling Wei,
  • Qiaohua Zheng,
  • Yanning Qiao,
  • Yihui Liu,
  • Wei Ren,
  • Jing Han,
  • Aozhuo Zhang,
  • Zhiqiang Liu,
  • Fei Gao

摘要

The body’s defensive emotional reaction to stress presents as anxiety. Nevertheless, long-term anxious stimuli can cause pathological anxiety disorders together with endocrine system, neural system, and immune system dysfunctions. Thus, researchers should understand the neural processes that govern anxiety during stress to create preventive and care plans. By combining behavioral tests, chemogenetic strategies, c-fos stainings, and whole-cell patch clamp recordings, this study looked into the function of dorsal medial prefrontal cortex (dmPFC) mu opioid receptors (MORs), specifically GABAergic MORs (MORGABA), in anxiety-like behavior brought on by acute restraint stress (ARS). The dmPFC MORGABA is triggered during ARS. This activation reduced the inhibitory synaptic input onto projection neurons that target the basolateral amygdala (BLA) by suppressing the activity of neighboring dmPFC GABAergic interneurons. In turn, mice that showed anxiety-like behavior also had higher neural activity of dmPFC-BLA projection neurons. When combined, these results describe a local, MORGABA-mediated dmPFC pathway that governs acute stress-induced anxiety reactions. These findings could offer a possible logical foundation for dmPFC-focused medication screening and anxiety treatment.