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特别表达在海马神经元中的BDNF与甲基神经毒性耐药性有关

Masatake Fujimura¹, Takamitsu Unoki¹

¹Department of Basic Medical Science, National Institute for Minamata Disease, Kumamoto, Japan.

Environmental toxicology

|February 7, 2024

概括

脑衍生神经营养因子 (BDNF),特别是在海马神经元 (HiNs) 中,赋予了对甲基 (MeHg) 神经毒性的抵抗力,可能是通过p44/42 MAPK通路和TrkB受体激活.

科学领域:

神经科学是一个神经科学.
神经生物学神经生物学神经生物学
毒理学毒理学毒理学

背景情况:

甲基 (MeHg) 选择性地损害大脑皮层神经元 (CCN),但不会损害海马神经元 (HiN).
大脑衍生神经营养因子 (BDNF) 特别表达在HiNs中,这表明它在神经保护中的作用.

研究的目的:

研究神经 (NTs) 包括BDNF在内的神经 (NTs) 在海马神经元 (HiNs) 与大脑皮层神经元 (CCNs) 的甲基 (MeHg) 抵抗中的作用.
阐明基因组中MeHg抗性的基础分子机制.

主要方法:

在培养的CCN和HiN中对NT蛋白表达和功能的比较分析.
利用小干扰RNAs (siRNAs) 来降低NT水平.
研究了p44/42中位素激活蛋白激酶 (MAPK) 途径的激活.
评估了外源BDNF和NT4/5对MeHg神经毒性的影响.

主要成果:

具体来说,BDNF是以HiN表达的,而其他NT则显示最小的差异表达.
在HiNs中减少BDNF减弱了MeHg抵抗和p44/42 MAPK激活.
外部添加BDNF和NT4/5通过TrkB受体激活抑制了两种神经元类型的MeHg神经毒性.
在HiNs中,p44/42 MAPK通路被构成性地激活.

结论:

具体表达为HiNs的BDNF在赋予对甲基 (MeHg) 神经毒性的耐药性方面发挥着至关重要的作用.
激活p44/42 MAPK通路与BDNF介导的对MeHg毒性的保护有关.
TrkB受体调解了BDNF和NT4/5对MeHg的神经保护作用.

关键词:

大脑皮层神经元的神经元海马神经元中的神经元甲基是一种.这些神经营养素是神经营养素 (neurotrophins).p44/42 马克········

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