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外部压力,甲和精神分裂症:一种新的小鼠模型用于精神疾病研究

Junhao Cheng^1,2, Zihui Sun^1,3, Hao Zhang¹

¹Zhejiang Provincial Clinical Research Center for Mental Disorders, The Affiliated Wenzhou Kangning Hospital, School of Mental Health, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, P.R. China.

Schizophrenia (Heidelberg, Germany)

|March 27, 2025

概括

压力产生甲 (FA),它阻断NMDA受体 (NMDARs) 并诱导小鼠的精神分裂症类似的行为. 这表明FA可能是精神分裂症的内源性触发因素.

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.
生物化学生物化学

背景情况:

NMDA受体 (NMDAR) 低功能是精神分裂症模型中的一个关键特征,通常由MK801.1诱导.
在精神分裂症中导致NMDAR抑制的确切内源因素尚不清楚.
外部压力与甲 (FA) 的产生有关,甲是一种已知的化合物,通过阻断NMDARs来损害认知功能.

研究的目的:

调查甲 (FA) 是否可以在小鼠模型中诱导精神分裂症类行为.
探索压力诱导的FA在精神分裂症病理生理学的作用.
建立一个新的小鼠模型用于使用FA微注射的精神分裂症.

主要方法:

在野生型小鼠中诱导了类似精神分裂症的症状,使用了各种方法,包括VTA刺激,将FA或TIQ微注入VTA,以及MK801的使用.
在前额皮层 (PFC) 和VTA中量化了FA和多巴胺 (DA) 的代谢水平.
使用高分辨率质谱 (HRMS) 和高性能液态染色学 (HPLC) 来确认TIQ的形成.
行为测试包括尾部悬浮,糖糖偏好,大理石埋葬,开放场地和Y迷宫测试.

主要成果:

外部压力和VTA刺激诱导了类似精神分裂症的行为,包括绝望,无情,刻板印象,焦虑和记忆缺陷.
这些行为与PFC和VTA的DA水平变化以及VTA的TIQ水平增加相关.
FA和DA的相互作用导致TIQ的形成,这本身就诱导了类似精神分裂症的症状.
FA微注射到VTA模仿MK801的影响,降低DA水平和PFC中的TH / MAO活性.

结论:

压力诱导的甲 (FA) 可以在小鼠中引发类似精神分裂症的行为.
通过其代谢物TIQ或直接作用,FA可能会作为精神分裂症发展的内生因素.
将FA微输入VTA提供了一种创新的方法,用于创建类似精神分裂症的小鼠模型.

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