Banei Farzin, Aliaghaei Abbas, Meftahi Gholam Hossein
Student Research Committee, Baqiyatallah University of Medical Sciences, Tehran, Iran.
Present Address: Department of Biology and Anatomical Sciences, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
3 Biotech. 2024 Oct;14(10):225. doi: 10.1007/s13205-024-04062-y. Epub 2024 Sep 6.
Oxycodone is widely used for pain management and acts via binding to mu- and kappa opioid receptors. It was shown that extended oxycodone usage can result from the demyelination and degeneration of neurons through the stress response, which triggers apoptotic signaling pathways. The striatum and cerebellum are recognized as significant contributors to addiction; however, there is no report on the effect of oxycodone on the cerebellum and striatum and motor coordination. We treated rats daily with oxycodone at 15 mg/kg doses for thirty days. Motor performance and electromyography activity were then evaluated. Stereological methods were performed to assess the number of neurons in the cerebellum and striatum as well as immunohistochemistry for microgliosis and astrogliosis. Furthermore, the Sholl analysis method was utilized to evaluate the cellular structure of both microglia and astrocytes. Results of the rotarod test for motor coordination show no significant ( < 0.05) difference between the oxycodone subjects and those in the control group. In addition, open-field assessments indicated that the application of oxycodone did not alter the amount of distance covered (as an indicator of locomotion) or time spent in the central area (as an indicator of anxiety) ( < 0.001). The electromyography (EMG) test result showed that oxycodone caused a delay in the reaction of the muscular nerves ( < 0.001). Data and results from our experiment revealed that administering oxycodone did not affect astrogliosis and the number of neurons in the cerebellum and striatum ( < 0.05). In contrast, it altered neuromuscular function. In addition, oxycodone administration activated microglia in the cerebellum and striatum. In conclusion, we encourage more research on the adverse effects of oxycodone on the brain.
羟考酮被广泛用于疼痛管理，通过与μ和κ阿片受体结合发挥作用。研究表明，长期使用羟考酮会通过应激反应导致神经元脱髓鞘和变性，进而触发细胞凋亡信号通路。纹状体和小脑被认为是成瘾的重要因素；然而，关于羟考酮对小脑、纹状体及运动协调的影响尚无报道。我们以15毫克/千克的剂量每日给大鼠注射羟考酮，持续30天。然后评估其运动表现和肌电图活动。采用体视学方法评估小脑和纹状体中的神经元数量，以及进行小胶质细胞增生和星形胶质细胞增生的免疫组织化学检测。此外，利用Sholl分析方法评估小胶质细胞和星形胶质细胞的细胞结构。运动协调的转棒试验结果显示，羟考酮处理组与对照组之间无显著差异（<0.05）。此外，旷场试验表明，使用羟考酮并未改变移动距离（作为运动指标）或在中央区域停留的时间（作为焦虑指标）（<0.001）。肌电图（EMG）测试结果表明，羟考酮导致肌肉神经反应延迟（<0.001）。我们实验的数据和结果显示，给予羟考酮不影响小脑和纹状体中的星形胶质细胞增生及神经元数量（<0.05）。相反，它改变了神经肌肉功能。此外，给予羟考酮会激活小脑和纹状体中的小胶质细胞。总之，我们鼓励对羟考酮对大脑的不良影响进行更多研究。
