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<p>Posttraumatic stress disorder (PTSD) is a devastating, prevalent psychological disorder characterized by excessive fear memory because of exposure to severe trauma. Stellate ganglion block (SGB) is traditionally used as a clinical treatment for pain but has been regarded as an innovative therapy for PTSD in recent reports. However, the mechanisms underlying the effect of SGB on PTSD remain unknown. Here, we established a fear conditioning model, which is considered a representative model of traumatic memory, and evaluated the effect of SGB on conditioned fear memory. We found that SGB reduced conditioned fear memory in mice in conjunction with the hypoactivity of locus coeruleus (LC) noradrenergic and basolateral amygdala (BLA) glutamatergic neurons. The norepinephrine concentration in the BLA decreased after SGB. Moreover, conditioned fear memory was re-enforced when the LC NE (LC<sup>NE</sup>)-BLA pathway was activated in SGB mice. Our study findings indicated that the hypoactivity of the LC<sup>NE</sup>-BLA pathway was the potential mechanism underlying the effects of SGB, which diminished consolidation of fear memory to relieve PTSD symptoms.</p>

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Stellate ganglion block diminishes consolidation of conditioned fear memory in mice by inhibiting the locus coeruleus to the basolateral amygdala neural circuit

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年5月17日

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  • Ziheng Wang,
  • Zhouliang Liu,
  • Youjia Yu,
  • Yuning Sun,
  • Yan Zhang,
  • Kailun Gao,
  • Junli Cao,
  • Liwei Wang,
  • Yangzi Zhu

摘要

Posttraumatic stress disorder (PTSD) is a devastating, prevalent psychological disorder characterized by excessive fear memory because of exposure to severe trauma. Stellate ganglion block (SGB) is traditionally used as a clinical treatment for pain but has been regarded as an innovative therapy for PTSD in recent reports. However, the mechanisms underlying the effect of SGB on PTSD remain unknown. Here, we established a fear conditioning model, which is considered a representative model of traumatic memory, and evaluated the effect of SGB on conditioned fear memory. We found that SGB reduced conditioned fear memory in mice in conjunction with the hypoactivity of locus coeruleus (LC) noradrenergic and basolateral amygdala (BLA) glutamatergic neurons. The norepinephrine concentration in the BLA decreased after SGB. Moreover, conditioned fear memory was re-enforced when the LC NE (LCNE)-BLA pathway was activated in SGB mice. Our study findings indicated that the hypoactivity of the LCNE-BLA pathway was the potential mechanism underlying the effects of SGB, which diminished consolidation of fear memory to relieve PTSD symptoms.