Department of Neurophysiology, Center for Brain Research, Medical University of Vienna, Vienna, Austria.
Mol Pain. 2011 Mar 28;7:20. doi: 10.1186/1744-8069-7-20.
Long-term potentiation (LTP) in nociceptive spinal pathways shares several features with hyperalgesia and has been proposed to be a cellular mechanism of pain amplification in acute and chronic pain states. Spinal LTP is typically induced by noxious input and has therefore been hypothesized to contribute to acute postoperative pain and to forms of chronic pain that develop from an initial painful event, peripheral inflammation or neuropathy. Under this assumption, preventing LTP induction may help to prevent the development of exaggerated postoperative pain and reversing established LTP may help to treat patients who have an LTP component to their chronic pain. Spinal LTP is also induced by abrupt opioid withdrawal, making it a possible mechanism of some forms of opioid-induced hyperalgesia. Here, we give an overview of targets for preventing LTP induction and modifying established LTP as identified in animal studies. We discuss which of the various symptoms of human experimental and clinical pain may be manifestations of spinal LTP, review the pharmacology of these possible human LTP manifestations and compare it to the pharmacology of spinal LTP in rodents.
伤害性脊髓通路的长时程增强（LTP）与痛觉过敏具有几个共同特征，并且已被提出作为急性和慢性疼痛状态下疼痛放大的细胞机制。脊髓 LTP 通常由有害刺激引起，因此被假设有助于急性术后疼痛和由初始疼痛事件、外周炎症或神经病变发展而来的慢性疼痛形式。根据这一假设，防止 LTP 诱导可能有助于预防术后疼痛的过度发展，而逆转已建立的 LTP 可能有助于治疗其慢性疼痛具有 LTP 成分的患者。脊髓 LTP 也由阿片类药物突然戒断引起，这使其成为某些形式的阿片类药物诱导痛觉过敏的可能机制。在这里，我们概述了在动物研究中确定的预防 LTP 诱导和修饰已建立的 LTP 的靶点。我们讨论了人类实验和临床疼痛的各种症状哪些可能是脊髓 LTP 的表现，回顾了这些可能的人类 LTP 表现的药理学，并将其与啮齿动物脊髓 LTP 的药理学进行了比较。
