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<p>Chronic pain and sleep disorders frequently co-occur and exacerbate each other, yet the neural mechanisms underlying this comorbidity remain poorly understood. Here, we found that hyperactivity of GABAergic neurons in the dorsal division of the lateral septum (LS<sup>GABA</sup>) drives both pain-like behavior and sleep disruption induced by spared nerve injury (SNI) in male mice. We showed that systemic or local application of dexmedetomidine (DEX), with known sedative and analgesic properties, reduces LS<sup>GABA</sup> hyperactivity via α<sub>2</sub>A adrenergic receptor activation, alleviating pain-like behavior and sleep disruption. LS<sup>GABA</sup> can project onto the glutamatergic and GABAergic neurons in the lateral preoptic area (LPO), respectively. The LS<sup>GABA</sup>→LPO<sup>Glu</sup> circuit and the LS<sup>GABA</sup> → LPO<sup>GABA</sup> circuit contribute to mechanical allodynia and sleep disruption, respectively. Furthermore, LS α<sub>2</sub>A adrenergic receptor plays an important role in DEX-regulated activity of LPO<sup>GABA</sup> and LPO<sup>Glu</sup>. Taken together, these findings reveal a shared neural substrate for chronic pain and sleep disorders and establish DEX as a potential treatment for this comorbidity through selective modulation of LS<sup>GABA</sup>-driven circuits.</p>

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Lateral septum GABAergic neurons mediate the effects of dexmedetomidine on allodynia and sleep in a male mouse model of neuropathic pain

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月19日

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  • Haiting Fan,
  • Yingying Su,
  • Jie Deng,
  • Zhengkai Liang,
  • Meiying Chen,
  • Kaibin Wu,
  • Peiwen Tang,
  • Chen Wang,
  • Deyi Kong,
  • Ting Xu,
  • Feixue Liang,
  • Wenjun Xin,
  • Yan Wu,
  • Xia Feng

摘要

Chronic pain and sleep disorders frequently co-occur and exacerbate each other, yet the neural mechanisms underlying this comorbidity remain poorly understood. Here, we found that hyperactivity of GABAergic neurons in the dorsal division of the lateral septum (LSGABA) drives both pain-like behavior and sleep disruption induced by spared nerve injury (SNI) in male mice. We showed that systemic or local application of dexmedetomidine (DEX), with known sedative and analgesic properties, reduces LSGABA hyperactivity via α2A adrenergic receptor activation, alleviating pain-like behavior and sleep disruption. LSGABA can project onto the glutamatergic and GABAergic neurons in the lateral preoptic area (LPO), respectively. The LSGABA→LPOGlu circuit and the LSGABA → LPOGABA circuit contribute to mechanical allodynia and sleep disruption, respectively. Furthermore, LS α2A adrenergic receptor plays an important role in DEX-regulated activity of LPOGABA and LPOGlu. Taken together, these findings reveal a shared neural substrate for chronic pain and sleep disorders and establish DEX as a potential treatment for this comorbidity through selective modulation of LSGABA-driven circuits.