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在SPS大鼠中,H₂S通过PI3K/AKT信号通路改善海马突触可塑性

Shuwen Yu¹, Wei Zhang², Xixi Wang¹

¹Department of Medical Psychology and Ethics, School of Basic Medicine Sciences, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250012, PR China.

|October 21, 2024

概括

单一的长期压力 (SPS),创伤后应激障碍 (PTSD) 的一个模型,降低了硫化 (H2S) 水平. 外源H2S的使用缓解了类似PTSD的行为,并通过调节PI3K/AKT通路改善了突触可塑性.

科学领域:

神经科学是一个神经科学.
精神病学是一个精神病学.
生物化学生化学

背景情况:

创伤后应激障碍 (PTSD) 是一种使人虚弱的精神疾病,其确切的治疗方法尚不清楚.
硫化 (H2S) 在精神疾病中起作用,但其在PTSD病原体中的参与尚不清楚.

研究的目的:

研究PTSD暴露对内源H2S水平的影响.
探索H2S水平和PTSD病原体之间的相关性.
为了确定外源H2S的管理是否可以改善PTSD类症状和改善突触可塑性.

主要方法:

利用单一长期压力 (SPS) 鼠标模型来模仿PTSD.
在SPS大鼠中测量了内源H2S含量.
给出了外源的H2S,并评估了行为变化和海马突触可塑性.
使用PI3K抑制剂LY294002.2.的PI3K/AKT/BDNF通路受到干扰.

主要成果:

SPS暴露降低了内源的H2S水平,导致异常行为和海马突触可塑性受损.
外源的H2S给药缓解了PTSD类行为,并增强了SPS大鼠的海马突触可塑性.
LY294002阻止了外源H2S对焦虑和突触可塑性的有益影响.

结论:

在PTSD鼠标模型中,内源H2S水平降低.
外源H2S可以缓解类似PTSD的疾病,并改善海马突触可塑性.
H2S的治疗作用通过PI3K/AKT通路进行介导.

关键词:

硫化是一种硫化.在PI3K/AKT信号通路中.创伤后应激障碍创伤后应激障碍突触性可塑性突触性可塑性

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