Przewlocki Ryszard, Przewlocka Barbara
Department of Molecular Neuropharmacology, Institute of Pharmacology, 12 Smetna Street, 31-343 Kraków, Poland.
Curr Pharm Des. 2005;11(23):3013-25. doi: 10.2174/1381612054865055.
Opiates lack potent analgesic efficacy in neuropathic pain although it is now generally accepted that the poor effect of these drugs reflects a reduction in their potency. Reduction of morphine antinociceptive potency was postulated to be due to the fact that nerve injury altered the activity of opioid systems or opioid specific signaling. Endogenous opioid systems were found to be represented in the regions involved in the nociception and are implicated in chronic pain. Opioid peptides biosynthesis and opioid receptors density in the nociceptive pathways and their functions change under various conditions associated with neuropathic pain following damage to the spinal cord and injury of peripheral nerves. Identification of a role of opioid systems in neuropathic pain and molecular and cellular mechanisms underlying these processes are of importance to understanding of the opioid action in neuropathic pain that will hopefully facilitate development of therapeutic strategies in which effectiveness of opioids in alleviation neuropathic pain is increased.
阿片类药物在神经性疼痛中缺乏强效镇痛效果,尽管现在人们普遍认为这些药物效果不佳反映了其效力的降低。吗啡抗伤害感受效力降低被推测是由于神经损伤改变了阿片系统或阿片特异性信号传导的活性。内源性阿片系统在参与伤害感受的区域中存在,并与慢性疼痛有关。在脊髓损伤和周围神经损伤后,与神经性疼痛相关的各种条件下,伤害感受通路中的阿片肽生物合成和阿片受体密度及其功能会发生变化。确定阿片系统在神经性疼痛中的作用以及这些过程背后的分子和细胞机制,对于理解阿片类药物在神经性疼痛中的作用非常重要,有望促进开发提高阿片类药物缓解神经性疼痛有效性的治疗策略。