Department of Psychology and Neuroscience, Center for Neuroscience, University of Colorado, Boulder, CO, USA.
Drug Design and Synthesis Section, National Institute on Alcohol Abuse and Alcoholism and National Institute on Drug Abuse, Bethesda, MD, USA.
J Neurosci Res. 2022 Jan;100(1):265-277. doi: 10.1002/jnr.24645. Epub 2020 Jun 13.
The present series of studies examine the impact of systemically administered therapeutics on peripheral nerve injury (males; unilateral sciatic chronic constriction injury [CCI])-induced suppression of voluntary wheel running, across weeks after dosing cessation. Following CCI, active phase running distance and speed are suppressed throughout the 7-week observation period. A brief course of morphine, however, increased active phase running distance and speed throughout this same period, an effect apparent only in sham rats. For CCI rats, systemic co-administration of morphine with antagonists of either P2X7 (A438079) or TLR4 ((+)-naloxone) (receptors critical to the activation of NLRP3 inflammasomes and consequent inflammatory cascades) returned running behavior of CCI rats to that of shams through 5+ weeks after dosing ceased. This is a striking difference in effect compared to our prior CCI allodynia results using systemic morphine plus intrathecal delivery of these same antagonists, wherein a sustained albeit partial suppression of neuropathic pain was observed. This may point to actions of the systemic drugs at multiple sites along the neuraxis, modulating injury-induced, inflammasome-mediated effects at the injured sciatic nerve and/or dorsal root ganglia, spinal cord, and potentially higher levels. Given that our data to date point to morphine amplifying neuroinflammatory processes put into motion by nerve injury, it is intriguing to speculate that co-administration of TLR4 and/or P2X7 antagonists can intervene in these inflammatory processes in a beneficial way. That is, that systemic administration of such compounds may suppress inflammatory damage at multiple sites, rapidly and persistently returning neuropathic animals to sham levels of response.
本系列研究探讨了系统给予治疗药物对周围神经损伤(雄性;单侧坐骨神经慢性缩窄性损伤[CCI])引起的自愿轮跑抑制的影响,即在停药后数周内。CCI 后,活跃期跑步距离和速度在 7 周观察期内受到抑制。然而,短期给予吗啡可增加活跃期跑步距离和速度,这一作用仅在假手术大鼠中出现。对于 CCI 大鼠,系统给予吗啡与 P2X7(A438079)或 TLR4((+)-naloxone)拮抗剂(对 NLRP3 炎性小体的激活和随后的炎症级联反应至关重要的受体)共同给药,可使 CCI 大鼠的跑步行为恢复到假手术组,持续 5 周以上。与我们之前使用全身吗啡和相同拮抗剂鞘内给药的 CCI 痛觉过敏结果相比,这是一个显著的效果差异,其中观察到持续但部分抑制神经性疼痛。这可能表明全身药物在沿神经轴的多个部位发挥作用,调节损伤诱导的、炎性小体介导的坐骨神经和/或背根神经节、脊髓以及潜在的更高水平的效应。鉴于我们目前的数据表明吗啡放大了神经炎症过程,由神经损伤引发,推测 TLR4 和/或 P2X7 拮抗剂的共同给药可以以有益的方式干预这些炎症过程。也就是说,系统给予这些化合物可能会在多个部位迅速而持久地抑制炎症性损伤,使神经病变动物迅速恢复到假手术水平的反应。