华盛顿大学医学院研究人员发现了大脑中的一种机制，可以有效控制慢性神经痛1。研究表明，位于脑部蓝斑核中的μ阿片受体能够充当生物"制动器"，通过抑制过度活跃的疼痛信号回路来关闭慢性神经痛1。这一发现为开发更加精准的慢性疼痛疗法提供了新的方向，有望避免全身使用阿片类药物所带来的副作用和成瘾风险1。
研究团队包括博士后研究员Chao-Cheng Kuo和前研究生Makenzie R. Norris，资深作者Jordan McCall指出："数百万成年人患有由神经损伤引起的慢性神经痛"1。在小鼠模型研究中，当科研人员从蓝斑核细胞中移除μ阿片受体后，动物对触觉和热痛的敏感性随之增加；而当他们恢复这些受体时，增加的敏感性得到逆转1。这项研究成果已于2026年8月17日发表在《当代生物学》期刊上1，相关研究工作获得了美国国立卫生研究院（NIH）、国家科学基金会（NSF）和McDonnell Center等多个机构的资金支持1。
Researchers at Washington University School of Medicine have discovered that μ-opioid receptors in the brain function as a biological "brake" capable of suppressing overactive pain circuits and shutting down chronic neuropathic pain 1. The findings, published in Current Biology on August 17, 2026, reveal that targeting these receptors in the locus coeruleus region of the brain could enable the development of more precise therapies for chronic pain while avoiding the systemic side effects and addiction risks associated with opioid medications 1.
The research team, including postdoctoral researcher Chao-Cheng Kuo and former graduate student Makenzie R. Norris, conducted studies in mouse models to understand this mechanism 1. When the scientists removed μ-opioid receptors from locus coeruleus cells, the animals displayed increased sensitivity to both tactile and thermal pain 1. Critically, when the researchers restored these receptors, the heightened pain sensitivity was reversed 1. Senior author Jordan McCall noted that "millions of adults suffer from chronic neuropathic pain caused by nerve injury," underscoring the clinical significance of the discovery 1.
The work was supported by multiple funding institutions including the National Institutes of Health (NIH), National Science Foundation (NSF), and the McDonnell Center 1.
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