星状神经节阻滞通过抑制杏仁核基底外侧神经回路的蓝斑,减少小鼠条件性恐惧记忆的巩固。

IF 6.2 1区 医学 Q1 PSYCHIATRY
Ziheng Wang, Zhouliang Liu, Youjia Yu, Yuning Sun, Yan Zhang, Kailun Gao, Junli Cao, Liwei Wang, Yangzi Zhu
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引用次数: 0

摘要

创伤后应激障碍(PTSD)是一种毁灭性的、普遍的心理障碍,其特征是由于暴露在严重的创伤中而产生过度的恐惧记忆。星状神经节阻滞(SGB)传统上用于临床治疗疼痛,但在最近的报道中被认为是治疗创伤后应激障碍的一种创新疗法。然而,SGB对PTSD的作用机制尚不清楚。在此,我们建立了一个创伤记忆的典型模型——恐惧条件反射模型,并评估了SGB对条件恐惧记忆的影响。我们发现SGB降低了小鼠的条件恐惧记忆,并伴有蓝斑(LC)去肾上腺素能和杏仁核基底外侧(BLA)谷氨酸能神经元的活性降低。SGB后BLA中去甲肾上腺素浓度降低。此外,激活lne -BLA通路后,条件恐惧记忆在SGB小鼠中得到强化。我们的研究结果表明lne - bla通路的低活性是SGB减少恐惧记忆巩固以缓解PTSD症状的潜在机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Stellate ganglion block diminishes consolidation of conditioned fear memory in mice by inhibiting the locus coeruleus to the basolateral amygdala neural circuit.

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.

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来源期刊
CiteScore
11.50
自引率
2.90%
发文量
484
审稿时长
23 weeks
期刊介绍: Psychiatry has suffered tremendously by the limited translational pipeline. Nobel laureate Julius Axelrod''s discovery in 1961 of monoamine reuptake by pre-synaptic neurons still forms the basis of contemporary antidepressant treatment. There is a grievous gap between the explosion of knowledge in neuroscience and conceptually novel treatments for our patients. Translational Psychiatry bridges this gap by fostering and highlighting the pathway from discovery to clinical applications, healthcare and global health. We view translation broadly as the full spectrum of work that marks the pathway from discovery to global health, inclusive. The steps of translation that are within the scope of Translational Psychiatry include (i) fundamental discovery, (ii) bench to bedside, (iii) bedside to clinical applications (clinical trials), (iv) translation to policy and health care guidelines, (v) assessment of health policy and usage, and (vi) global health. All areas of medical research, including — but not restricted to — molecular biology, genetics, pharmacology, imaging and epidemiology are welcome as they contribute to enhance the field of translational psychiatry.
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