Unraveling the role of oligodendrocytes and myelin in pain.

IF 4.2 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Journal of Neurochemistry Pub Date : 2024-08-20 DOI:10.1111/jnc.16206
Woojin Kim, María Cecilia Angulo
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Abstract

Oligodendrocytes, the myelin-producing cells in the central nervous system (CNS), are crucial for rapid action potential conduction and neuronal communication. While extensively studied for their roles in neuronal support and axonal insulation, their involvement in pain modulation is an emerging research area. This review explores the interplay between oligodendrocytes, myelination, and pain, focusing on neuropathic pain following peripheral nerve injury, spinal cord injury (SCI), chemotherapy, and HIV infection. Studies indicate that a decrease in oligodendrocytes and increased cytokine production by oligodendroglia in response to injury can induce or exacerbate pain. An increase in endogenous oligodendrocyte precursor cells (OPCs) may be a compensatory response to repair damaged oligodendrocytes. Exogenous OPC transplantation shows promise in alleviating SCI-induced neuropathic pain and enhancing remyelination. Additionally, oligodendrocyte apoptosis in brain regions such as the medial prefrontal cortex is linked to opioid-induced hyperalgesia, highlighting their role in central pain mechanisms. Chemotherapeutic agents disrupt oligodendrocyte differentiation, leading to persistent pain, while HIV-associated neuropathy involves up-regulation of oligodendrocyte lineage cell markers. These findings underscore the multifaceted roles of oligodendrocytes in pain pathways, suggesting that targeting myelination processes could offer new therapeutic strategies for chronic pain management. Further research should elucidate the underlying molecular mechanisms to develop effective pain treatments.

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揭示少突胶质细胞和髓鞘在疼痛中的作用。
少突胶质细胞是中枢神经系统(CNS)中产生髓鞘的细胞,对动作电位的快速传导和神经元的交流至关重要。人们对少突胶质细胞在神经元支持和轴突绝缘中的作用进行了广泛的研究,而它们在疼痛调节中的参与则是一个新兴的研究领域。这篇综述探讨了少突胶质细胞、髓鞘化和疼痛之间的相互作用,重点是周围神经损伤、脊髓损伤(SCI)、化疗和艾滋病病毒感染后的神经性疼痛。研究表明,少突胶质细胞因损伤而减少,细胞因子分泌增加,可诱发或加剧疼痛。内源性少突胶质前体细胞(OPC)的增加可能是修复受损少突胶质细胞的一种代偿反应。外源性少突胶质细胞前体细胞移植有望减轻 SCI 引起的神经性疼痛并促进髓鞘再形成。此外,内侧前额叶皮层等脑区的少突胶质细胞凋亡与阿片类药物诱发的痛觉减退有关,这突显了它们在中枢疼痛机制中的作用。化疗药物会破坏少突胶质细胞的分化,从而导致持续性疼痛,而艾滋病毒相关神经病则涉及少突胶质细胞系细胞标记的上调。这些发现强调了少突胶质细胞在疼痛通路中的多方面作用,表明针对髓鞘化过程可为慢性疼痛治疗提供新的治疗策略。进一步的研究应阐明潜在的分子机制,以开发有效的疼痛治疗方法。
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来源期刊
Journal of Neurochemistry
Journal of Neurochemistry 医学-神经科学
CiteScore
9.30
自引率
2.10%
发文量
181
审稿时长
2.2 months
期刊介绍: Journal of Neurochemistry focuses on molecular, cellular and biochemical aspects of the nervous system, the pathogenesis of neurological disorders and the development of disease specific biomarkers. It is devoted to the prompt publication of original findings of the highest scientific priority and value that provide novel mechanistic insights, represent a clear advance over previous studies and have the potential to generate exciting future research.
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