Bach F W
Department of Neurology, National University Hospital, Copenhagen, Denmark.
Acta Anaesthesiol Scand. 1997 Jan;41(1 Pt 2):133-40. doi: 10.1111/j.1399-6576.1997.tb04627.x.
We have known the endogenous opioid peptide beta-endorphin for 20 years. Surprisingly, our knowledge of the physiological role of this peptide and its receptors in modulation of pain perception is still fragmentary. Whereas most studies have tried to elucidate the physiological role of beta-endorphin by reversing evoked responses by the opioid antagonist naloxone, this review focuses on quantification of release of beta-endorphin in the brain as the approach to define physiological and pathophysiological roles of beta-endorphin in relation to nociception. Using a lateral ventricle-cisterna magna perfusion model in the anesthetized rat, it was shown that depolarization of neurons in the arcuate nucleus of the hypothalamus, where beta-endorphin in produced, was followed by release of beta-endorphin to the cerebrospinal fluid compartment. Intense activation of spinal nociceptive pathways by intrathecal capsaicin injections also led to beta-endorphin release. It is concluded that there may still be good reason to quantify beta-endorphin in human cerebrospinal fluid to elucidate the role of beta-endorphin in pain perception.
我们认识内源性阿片肽β-内啡肽已有20年了。令人惊讶的是，我们对这种肽及其受体在调节疼痛感知方面的生理作用的了解仍然支离破碎。尽管大多数研究试图通过阿片拮抗剂纳洛酮逆转诱发反应来阐明β-内啡肽的生理作用，但本综述重点关注脑内β-内啡肽的释放定量，以此作为确定β-内啡肽在伤害感受方面的生理和病理生理作用的方法。在麻醉大鼠中使用侧脑室-大池灌注模型，结果显示，在下丘脑弓状核（β-内啡肽在此产生）的神经元去极化后，β-内啡肽会释放到脑脊液腔室中。鞘内注射辣椒素强烈激活脊髓伤害性感受通路也会导致β-内啡肽释放。得出的结论是，为了阐明β-内啡肽在疼痛感知中的作用，仍有充分的理由对人脑脊液中的β-内啡肽进行定量分析。
