Galanin up-regulates the expression of M1 muscarinic acetylcholine receptor via the ERK signaling pathway in primary cultured prefrontal cortical neurons. (17th March 2015)

• Record Type: Journal Article
• Authors: Cheng, Yong; Yu, Long-Chuan
• Is Part Of: Neuroscience letters. Volume 590(2015)
• Page Start: 161
• Page End: 165
• Publication Date: 2015-03-17
• Subjects: Galanin -- M1 muscarinic acetylcholine receptor -- Alzheimer's disease -- ERK; Neurology -- Periodicals; Neurology -- Periodicals; Research -- Periodicals; Neurologie -- Périodiques; Neuroanatomie -- Périodiques; Neuropharmacologie -- Périodiques; Neurophysiologie -- Périodiques; Neurology; Periodicals; Electronic journals; 617.48
• DOI: 10.1016/j.neulet.2015.02.011
• Languages: English
• ISSNs: 0304-3940

Abstract

Highlights: Galanin up-regulates the expression of M1 receptor in the neurons. The ERK signaling pathway mediates the galanin induced up-regulation of M1 receptor. Our study supports the hypothesis that galanin is neurotrophic in the progress of AD. Abstract: 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.