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准后突触支架蛋白PSD-95增强了BDNF信号传递,以减轻小鼠的类似抑郁症的行为

Xin Shi¹, Xiao-Zhong Zhou^1,2, Gang Chen³

¹Clinical Research Center of Neurological Disease, Second Affiliated Hospital of Soochow University, Institution of Neuroscience, Soochow University, Suzhou 215123, China.

Science signaling

|April 30, 2024

概括

针对PSD-95的新化合物促进脑衍生神经营养因子 (BDNF) 信号传递,通过减少小鼠的抑郁症行为来提供潜在的抗抑郁作用.

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
药理学药理学是指药理学的学科.

背景情况:

在临床抑郁症中,对神经元功能至关重要的脑衍生神经营养因子 (BDNF) 信号发送受损.
后突触支架蛋白PSD-95在支持BDNF信号传递方面发挥着作用.

研究的目的:

调查针对PSD-95.5的新型皮多米米特化合物的抗抑郁潜力.
阐明这些化合物对类似抑郁症的行为产生治疗效应的分子机制.

主要方法:

利用压力诱导抑郁症的小鼠模型.
已使用的针对PSD-95.5的胺基化合物 (CN2097和Syn3).
评估了类似抑郁症的行为,海马体信号通路 (PI3K-Akt-mTOR),神经元形态和自.
研究了Gα_i1/3和TrkB受体信号传递的作用.

主要成果:

结合PSD-95的化合物CN2097和Syn3促进了海马体中BDNF受体TrkB信号传递.
在压力诱导抑郁症的小鼠模型中,Syn3显著减少了类似抑郁症的行为.
Syn3增强了TrkB-Gα_i1/3-PSD-95复合体的形成,并强化了PI3K-Akt-mTOR信号,扭转了压力引起的变化.
Syn3的治疗效果取决于Gα_i1/3和TrkB通路的激活.

结论:

促进PSD-95-TrkB复合体形成的化合物具有显著的抗抑郁药物潜力.
针对PSD-95提供了一种通过调节BDNF信号通路来治疗抑郁症的新治疗策略.

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