Cortical regulation of striatal projection neurons and interneurons in a Parkinson's disease rat model

作     者：Jia-jia Wu Si Chen Li-si Ouyang Yu Jia Bing-bing Liu Shu-hua Mu Yu-xin Ma Wei-ping Wang Jia-you Wei You-lan Li Zhi Chen Wan-long Lei 

作者机构：Department of AnatomyZhongshan School of MedicineSun Yat-sen University Periodical Centerthe Third Affiliated HospitalSun Yat-sen University Department of AnesthesiologyGuangdong No.2 Provincial People’s HospitalGuangdong Provincial Emergency Hospital Key Laboratory of Optoelectronic Devices and Systems of Ministry of Education and Guangdong ProvinceCollege of Optoelectronic EngineeringShenzhen University 

出 版 物：《Neural Regeneration Research》 (中国神经再生研究（英文版）)

年 卷 期：2016年第11卷第12期

页      面：1969-1975页

核心收录：

学科分类：1002[医学-临床医学] 100204[医学-神经病学] 10[医学] 

基　　金：supported by the National Natural Science Foundation of China No.81471288 

主　　题：nerve regeneration motor cortex lesions dopaminergic neurons GABAergic neurons Darpp32 calbindin μ opioid receptor neuropeptide Y parvalbumin neural regeneration 

摘      要：Striatal neurons can be either projection neurons or interneurons, with each type exhibiting distinct susceptibility to various types of brain damage. In this study, 6-hydroxydopamine was injected into the right medial forebrain bundle to induce dopamine depletion, and/or ibotenic acid was injected into the M1 cortex to induce motor cortex lesions. Immunohistochemistry and western blot assay showed that dopaminergic depletion results in significant loss of striatal projection neurons marked by dopamine- and cyclic adenosine monophosphate-regulated phosphoprotein, molecular weight 32 k Da, calbindin, and μ-opioid receptor, while cortical lesions reversed these pathological changes. After dopaminergic deletion, the number of neuropeptide Y-positive striatal interneurons markedly increased, which was also inhibited by cortical lesioning. No noticeable change in the number of parvalbumin-positive interneurons was found in 6-hydroxydopamine-treated rats. Striatal projection neurons and interneurons show different susceptibility to dopaminergic depletion. Further, cortical lesions inhibit striatal dysfunction and damage induced by 6-hydroxydopamine, which provides a new possibility for clinical treatment of Parkinson＇s disease.