Zhang WJ, Shi LL, Zhang L. Dysregulated cortical synaptic plasticity under methyl-CpG binding protein 2 deficiency and its implication in motor impairments. World J Psychiatry 2022; 12(5): 673-682 [PMID: 35663301 DOI: 10.5498/wjp.v12.i5.673]
Corresponding Author of This Article
Li Zhang, PhD, Associate Professor, GHM Institute of CNS Regeneration, Jinan University, No. 601 Huangpu Avenue West, Guangzhou 510632, Guangdong Province, China. zhangli@jnu.edu.cn
Research Domain of This Article
Neurosciences
Article-Type of This Article
Minireviews
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Psychiatry. May 19, 2022; 12(5): 673-682 Published online May 19, 2022. doi: 10.5498/wjp.v12.i5.673
Dysregulated cortical synaptic plasticity under methyl-CpG binding protein 2 deficiency and its implication in motor impairments
Wei-Jia Zhang, Ling-Ling Shi, Li Zhang
Wei-Jia Zhang, Ling-Ling Shi, Li Zhang, GHM Institute of CNS Regeneration, Jinan University, Guangzhou 510632, Guangdong Province, China
Author contributions: Zhang WJ and Zhang L prepared the literature reviews and drafted the manuscript with input by Shi LL; Shi LL and Zhang L revised the manuscript and approved it.
Supported bythe National Natural Science Foundation of China, No. 81771222; the Guangdong Province Basic and Applied Basic Research Fund Project, No. 2019A1515011316; and the Guangzhou Science and Technology Plan Project, No. 202007030011.
Conflict-of-interest statement: All authors declare no competing interests.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Li Zhang, PhD, Associate Professor, GHM Institute of CNS Regeneration, Jinan University, No. 601 Huangpu Avenue West, Guangzhou 510632, Guangdong Province, China. zhangli@jnu.edu.cn
Received: April 15, 2021 Peer-review started: April 15, 2021 First decision: June 17, 2021 Revised: July 16, 2021 Accepted: April 1, 2022 Article in press: April 1, 2022 Published online: May 19, 2022 Processing time: 397 Days and 18.8 Hours
Abstract
Caused by the mutation of methyl-CpG binding protein 2 (MeCP2), Rett syndrome leads to a battery of severe neural dysfunctions including the regression of motor coordination and motor learning. Current understanding has revealed the motor cortex as the critical region mediating voluntary movement. In this review article, we will summarize major findings from human patients and animal models regarding the cortical synaptic plasticity under the regulation of MeCP2. We will also discuss how mutation of MeCP2 leads to the disruption of cortical circuitry homeostasis to cause motor deficits. Lastly, potential values of physical exercise and neuromodulation approaches to recover neural plasticity and motor function will be evaluated. All of this evidence may help to accelerate timely diagnosis and effective interventions for Rett syndrome patients.
Core Tip: In this mini-review, Zhang WJ summarized current findings for the synaptic plasticity in the cortex and related motor learning functions under the scenario of Rett syndrome. The discussion of neuropathological mechanisms can help us to better understand the disease progression and more importantly to develop more effective measures to counteract motor deficits.
