Research Center of Physiology, Semnan University of Medical Sciences, Semnan, Iran.
Student Research Committee, Semnan University of Medical Sciences, Semnan, Iran.
Neurol Res. 2024 Apr;46(4):330-338. doi: 10.1080/01616412.2024.2313901. Epub 2024 Feb 7.
The pain-reducing effects of the exercise were exerted through different mechanisms. Knowing more clear mechanisms helps to find more approach that is therapeutic. The objective of the present study is the evaluation of cerebrospinal fluid (CSF) glutamate level alteration in neuropathic pain rats and whether physical activity could modulate it.
In the present study 104 male rats weighing 180-220 g were randomly divided into 4 groups (Sham, Sham + Exe, Neuropathy, and Neuropathy + Exe) which in turn each group subdivided into 4 groups according to time points for behavioral testing and CSF sampling (Baseline, 2 weeks, 3 weeks, and 4 weeks). To induction of neuropathy (by chronic constriction injury,), after anesthetizing with a mixture of ketamine (80 mg/kg) and xylazine (10 mg/kg), the animal's right sciatic nerve was exposed and was ligated using four movable catgut chromic suture 4/0. The exercise protocol included 25 min of daily swimming, 5 days a week for 4 weeks. Thermal hyperalgesia and mechanical tactile threshold were detected using the plantar test and Von Frey filaments, respectively. CSF glutamate level was determined using high-performance liquid chromatography.
Findings indicated that mechanical and thermal thresholds significantly ( < 0.01, < 0.05 respectively) decreased in the neuropathy group against that in sham groups. On the other hand, exercise significantly increased mechanical tactile threshold ( < 0.0012) and thermal threshold ( < 0.05) compared to the neuropathy group. Moreover, CSF glutamate level prominently ( < 0.01) was increased in the neuropathy group compared to the sham group, and swimming exercise significantly ( < 0.001) reduced it.
The present findings provide new evidence showing that medium-intensity swimming exercise attenuates pain-like behaviors in neuropathic pain animals, which is possibly due to decreasing CSF glutamate level and its neurotransmission.
运动的止痛作用是通过不同的机制发挥的。了解更明确的机制有助于找到更多的治疗方法。本研究的目的是评估神经病理性疼痛大鼠脑脊液(CSF)谷氨酸水平的改变,以及体育活动是否能调节这种改变。
本研究将 104 只体重为 180-220 克的雄性大鼠随机分为 4 组(假手术组、假手术+运动组、神经病理性疼痛组和神经病理性疼痛+运动组),每组又根据行为测试和 CSF 取样的时间点分为 4 组(基线、2 周、3 周和 4 周)。为了诱导神经病理性疼痛(通过慢性缩窄性损伤),在使用混合的氯胺酮(80 毫克/公斤)和甲苯噻嗪(10 毫克/公斤)麻醉后,暴露动物的右侧坐骨神经,并使用 4 根可移动的肠线铬缝线 4/0 结扎。运动方案包括每天游泳 25 分钟,每周 5 天,共 4 周。使用足底测试和 Von Frey 纤维分别检测热痛觉过敏和机械触觉阈值。使用高效液相色谱法测定 CSF 谷氨酸水平。
结果表明,与假手术组相比,神经病理性疼痛组的机械和热阈值显著(<0.01,<0.05)降低。另一方面,与神经病理性疼痛组相比,运动显著增加了机械触觉阈值(<0.0012)和热阈值(<0.05)。此外,与假手术组相比,神经病理性疼痛组的 CSF 谷氨酸水平显著升高(<0.01),而游泳运动显著降低了其水平(<0.001)。
本研究结果提供了新的证据,表明中等强度的游泳运动可减轻神经病理性疼痛动物的疼痛样行为,这可能是由于降低了 CSF 谷氨酸水平及其神经传递。