Cheng Yong, Yu Long-Chuan
Laboratory of Neurobiology and State Key Laboratory of Biomembrane and Membrane Biotechnology, College of Life Sciences, Peking University, Beijing 100871, China.
Laboratory of Neurobiology and State Key Laboratory of Biomembrane and Membrane Biotechnology, College of Life Sciences, Peking University, Beijing 100871, China.
Neurosci Lett. 2015 Mar 17;590:161-5. doi: 10.1016/j.neulet.2015.02.011. Epub 2015 Feb 9.
The expression of galanin and galanin receptors are up-regulated in the brains from patients with Alzheimer's disease (AD). However, the role of galanin in the progress of AD is still controversial. Here we demonstrated that galanin increased the protein expression of M1 muscarinic acetylcholine receptor (M1) in the primary cultured prefrontal cortical neurons by ELISA and Western Blot. Moreover, we showed that the mRNA expression of M1 was also up-regulated by galanin treatment. We further explored the mechanism of the galanin induced up-regulation of M1. We found that galanin activated the ERK signaling pathway in the primary cultured prefrontal cortical neurons. In addition, our results showed that the up-regulation of M1 mRNA was blocked by an ERK inhibitor, U0126. Taken together, our results demonstrated that the ERK signaling pathway mediated the galanin induced up-regulation of M1 in the primary cultured prefrontal cortical neurons, supporting the hypothesis that galanin plays a beneficial role in the development of AD.
在阿尔茨海默病（AD）患者的大脑中，甘丙肽及其受体的表达上调。然而，甘丙肽在AD进展中的作用仍存在争议。在此，我们通过酶联免疫吸附测定（ELISA）和蛋白质免疫印迹法（Western Blot）证明，甘丙肽可增加原代培养的前额叶皮质神经元中M1毒蕈碱型乙酰胆碱受体（M1）的蛋白表达。此外，我们还表明，甘丙肽处理也可上调M1的mRNA表达。我们进一步探究了甘丙肽诱导M1上调的机制。我们发现，甘丙肽可激活原代培养的前额叶皮质神经元中的细胞外信号调节激酶（ERK）信号通路。此外，我们的结果表明，ERK抑制剂U0126可阻断M1 mRNA的上调。综上所述，我们的结果表明，ERK信号通路介导了甘丙肽诱导的原代培养的前额叶皮质神经元中M1的上调，支持了甘丙肽在AD发展中发挥有益作用这一假说。
