Changed cholinergic system and neuronal signal transduction in the rats with deficit of learning and memory induced by chronic fluorosis

Authors: Zhi-Zhong Guan^ab, Yan-Jie Liu^a, Chuan-Zhi Gui^b, Long-Yan Ran^a and Qin Gao^b

Correspondence: Professor Zhi-Zhong Guan, ^aDepartment of Pathology and ^bThe Key Lab of Molecular Biology in Guiyang Medical University, Guiyang 550004, P.R. China

E-mail: [email protected]

In order to reveal the mechanism of the decreased ability of learning and memory induced by chronic fluorosis, nicotinic acetylcholine receptors (nAChRs), cholinesterase (ChE) activity, and the pathway of extracellular signal regulated protein kinase (ERK1/2) were investigated by using the rats with chronic fluorosis including water pollution type and coal-burning pollution type. Spatial learning and memory of the rats were evaluated by Morris Water Maze test. The expressions of nAChRs, ERK1/2 and mitogen-induced extracellular kinase (MEK1/2) at protein and mRNA levels were detected by Western blotting and Real-time PCR, respectively. ChE activity was determined by chemical colorimetry. The results showed that the learning and memory capacity in the rats with chronic fluorosis was decreased. In the brain tissues from teh rats with fluorosis as compared to controls, the protein expressions of nAChR subunits were declined and the corresponding mRNAs of these receptor subunits changed; the activities of acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) were reduced; the increases of phospho-ERK1/2 and -MEK1/2 at the protein level but no change of ERK1/2 mRNA were found, and the activation rate of phospho-ERK1/2 was decreased. The modifications of nAChRs and ERK1/2 pathway might be connected with the molecular mechanism in the decreased ability of learning and memory of the rats influenced by chronic fluorosis.

Keywords: Fluorosis; Learning and memory; nAChRs; Rats;

Signal transduction

• Legal notice:
  

  Copyright (c) Pielaszek Research, all rights reserved.
  The above materials, including auxiliary resources, are subject to Publisher's copyright and the Author(s) intellectual rights. Without limiting Author(s) rights under respective Copyright Transfer Agreement, no part of the above documents may be reproduced without the express written permission of Pielaszek Research, the Publisher. Express permission from the Author(s) is required to use the above materials for academic purposes, such as lectures or scientific presentations.
  In every case, proper references including Author(s) name(s) and URL of this webpage: https://science24.com/paper/28171 must be provided.