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慢性术后疼痛诱导背景恐惧灭绝功能障碍通过海马NMDAR/BDNF/TrkB信号通路在小鼠

Jiawei Zhang^1,2, Xiaoting Zheng³, Gaoyan Zhang^1,2

¹Department of Anesthesiology, the First Affiliated Hospital of Anhui Medical University, Hefei, Anhui Province, 230022, China.

Translational psychiatry

|June 17, 2025

概括

手术后的疼痛通过降低大脑通路的调节,损害了恐惧的灭绝. 恢复这些通路可能有助于治疗同时出现的慢性疼痛和PTSD.

科学领域:

神经科学是一个神经科学.
分子生物学分子生物学
精神病学是一个精神病学.

背景情况:

创伤后应激障碍 (PTSD) 通常涉及恐惧灭绝功能障碍.
术后持续性疼痛会对生活质量产生负面影响,并与PTSD相关.
关联慢性疼痛和PTSD的分子机制,特别是恐惧灭绝,尚不清楚.

研究的目的:

调查海马体N-甲基-D-酸盐谷氨酸受体 (NMDARs) 和来自大脑的神经营养因子 (BDNF) 在术后疼痛后恐惧灭绝信号中的作用.
探索慢性疼痛和PTSD之间的共同疾病的分子基础.

主要方法:

建立了一种皮肤/肌肉切割和收缩 (SMIR) 鼠标模型,以模拟术后持续疼痛.
将NMDARs激动剂 (NMDA) 和TrkB抑制剂 (ANA-12) 输入海马.
评估了情境恐惧灭绝,记忆检索,突触可塑性以及NMDARs/ERK/CREB/BDNF信号通路.

主要成果:

SMIR小鼠表现出受损的上下文恐惧灭绝,与下调的海马体NMDARs/ERK/CREB/BDNF信号传递和降低的突触可塑性有关.
河马NMDA的管理通过激活信号通路和恢复树突状脊柱,改善了恐惧灭绝学习和记忆检索.
同时服用NMDA和ANA-12可以增强学习能力,但不能恢复,并重新诱导脊柱损失.

结论:

术后持续性疼痛通过降低NMDARs/ERK/CREB/BDNF通路的调节来破坏突触可塑性,导致情境恐惧灭绝功能障碍.
这些发现提供了关于慢性疼痛和PTSD共同疾病背后的机制的见解.

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