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产前低剂量Bisphenol A暴露会通过后代的cAMP-PKA-CREB通路影响皮质发育

Chu Jiang^1,2,3, Jun Guan^1,2,3, Xiangrong Tang⁴

¹Furong Laboratory, Center for Medical Genetics, School of Life Sciences, Central South University, Changsha, Hunan, China.

Frontiers in integrative neuroscience

|August 22, 2024

概括

产前暴露于低剂量的双A (BPA) 会改变大脑发育,并导致后代的躁狂行为. 这些效应与cAMP-PKA-CREB通路的过度激活有关,这表明PKA在BPA中起着关键作用.

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
毒理学毒理学毒理学

背景情况:

双A (BPA) 是一种常见的增塑剂,与健康障碍有关.
产前低剂量BPA暴露,即使低于安全限值,也可能导致儿童的神经和行为缺陷.
BPA对神经发育的影响背后的机制尚未完全理解.

研究的目的:

调查产前低剂量BPA暴露对皮质神经元发育的影响.
阐明参与BPA诱导的神经发育和行为变化的分子途径.
评估cAMP-PKA-CREB通路在调解这些影响中的作用.

主要方法:

孕妇暴露于低剂量的BPA.孕妇暴露于低剂量的BPA.
对后代皮层神经元增殖和迁移的分析.
转录组分析 (RNA测序) 以确定受影响的途径.
使用H89.9进行蛋白激酶A (PKA) 的药理抑制.

主要成果:

产前BPA暴露增加了皮质神经元数量,增殖和减少迁移.
RNA测序揭示了cAMP-PKA-CREB通路的异常激活.
抑制PKA (H89) 挽救了神经元增殖和迁移缺陷.
暴露于BPA的后代表现出类似躁狂的行为 (过度活跃,类似抗抑郁药,减少焦虑);H89正常化过度活跃.

结论:

过度激活PKA是BPA诱导的神经元发育变化的关键媒介.
产前低剂量BPA暴露会导致持续的神经发育和行为变化.
躁狂类行为可能是神经元发育改变和PKA信号的结合.

关键词:

BPA BPA BPA BPA BPA BPA BPA BPA BPA BPA BPA BPA BPA BPA BPA BPA BPA BPA BPA BPA BPA BPA BPA BPA BPA BPA BPA BPA BPA BPA BPA BPA BPA BPA 在cAMP-PKA-CREB路径中.类似躁狂的行为神经元迁移的神经元迁移神经元的扩散是神经元的扩散.在产前低剂量暴露.

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