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在自闭症的实验模型中,伴随着元可塑性的遗传机器以不同的方式运作
Esra Tufan Benli1, Ercan Babur2, Nurcan Dursun2
1Faculty of Medicine, Department of Physiology, Institute of Health Sciences COHE 100/2000 Doctorate Program, Human Brain and Neuroscience Sub-Field, Recites University, Kayseri, Turkey.
概括
在怀孕的老鼠中暴露于烯酸 (VPA) 会损害后代.
科学领域:
- 神经科学是一个神经科学.
- 发展生物学 发展生物学
- 遗传学 遗传学 是一个
背景情况:
- 怀孕期间暴露于酸 (VPA) 与后代患自闭症谱系障碍 (ASD) 的风险增加有关.
- 超可塑性,即突触可塑性的活动依赖调节,在学习和记忆中起着至关重要的作用.
- PI3K/AKT通路与神经元发育和突触功能有关.
研究的目的:
- 为了研究产前VPA暴露对海马体内超塑性相关基因表达的影响.
- 为了检查VPA治疗大鼠后代的行为缺陷和突触可塑性.
- 探索PI3K/AKT途径在VPA诱导的神经发育变化的作用.
主要方法:
- 在怀孕期间,威斯塔尔母接受了VPA或盐水.
- 后代接受了行为测试 (网格行走,负地质测试,社交互动) 和突触可塑性 (场刺激后突触潜力) 的电生理学评估.
- 使用定量实时PCR (rt-PCR) 来测量海马体PI3K,PTEN,AKT,GSK-3β和MAPT的mRNA水平.
主要成果:
- VPA后代表现出受损的感觉运动协调,减少社交能力,以及社会新奇事物偏好的缺陷.
- 电生理学发现,在VPA后代中,场刺激后突触潜能 (fEPSP) 斜率的输入输出曲线减少.
- 虽然代塑性反应相似,但PI3K/AKT通路基因的mRNA水平在VPA后代的诱导后下调.
结论:
- 产前VPA暴露会在男性后代中引起持久的行为和突触缺陷.
- 下调PI3K/AKT通路基因可能会导致VPA诱导的神经发育变化.
- 这些发现表明,一种适应机制涉及基因表达的变化,在对长期增强的元塑性控制过程中,作为对VPA暴露的反应.
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