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帕金森病相关慢性痛的细胞和突触机制。

Cellular and synaptic mechanisms for Parkinson's disease-related chronic pain.

机构信息

Institute for Brain Research, Qingdao International Academician Park, Qingdao, China.

Center for Neuron and Disease, Frontier Institute of Science and Technology, Xi'an Jiaotong University, Xi'an, China.

出版信息

Mol Pain. 2021 Jan-Dec;17:1744806921999025. doi: 10.1177/1744806921999025.

DOI:10.1177/1744806921999025
PMID:33784837
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8020085/
Abstract

Parkinson's disease is the second most common neurodegenerative disorder after Alzheimer's disease. Chronic pain is experienced by the vast majority of patients living with Parkinson's disease. The degeneration of dopaminergic neuron acts as the essential mechanism of Parkinson's disease in the midbrain dopaminergic pathway. The impairment of dopaminergic neurons leads to dysfunctions of the nociceptive system. Key cortical areas, such as the anterior cingulate cortex (ACC) and insular cortex (IC) that receive the dopaminergic projections are involved in pain transmission. Dopamine changes synaptic transmission via several pathway, for example the D2-adenly cyclase (AC)-cyclic AMP (cAMP)-protein kinase A (PKA) pathway and D1-G protein-coupled receptor kinase 2 (GRK2)-fragile X mental retardation protein (FMRP) pathway. The management of Parkinson's disease-related pain implicates maintenance of stable level of dopaminergic drugs and analgesics, however a more selective drug targeting at key molecules in Parkinson's disease-related pain remains to be investigated.

摘要

帕金森病是仅次于阿尔茨海默病的第二大常见神经退行性疾病。绝大多数帕金森病患者都经历过慢性疼痛。中脑多巴胺能通路中的多巴胺能神经元退化是帕金森病的基本机制。多巴胺能神经元的损伤导致伤害感受系统的功能障碍。接收多巴胺能投射的关键皮质区域,如前扣带皮层(ACC)和岛叶皮层(IC),参与疼痛传递。多巴胺通过几种途径改变突触传递,例如 D2-腺苷酸环化酶(AC)-环磷酸腺苷(cAMP)-蛋白激酶 A(PKA)途径和 D1-G 蛋白偶联受体激酶 2(GRK2)-脆性 X 智力迟钝蛋白(FMRP)途径。帕金森病相关疼痛的管理需要维持稳定的多巴胺能药物和镇痛药水平,然而,针对帕金森病相关疼痛关键分子的更具选择性的药物仍有待研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efca/8020085/236c2819495a/10.1177_1744806921999025-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efca/8020085/3606c6567c89/10.1177_1744806921999025-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efca/8020085/29dce6de54cf/10.1177_1744806921999025-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efca/8020085/236c2819495a/10.1177_1744806921999025-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efca/8020085/3606c6567c89/10.1177_1744806921999025-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efca/8020085/29dce6de54cf/10.1177_1744806921999025-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efca/8020085/236c2819495a/10.1177_1744806921999025-fig3.jpg

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