Bhattacharyya Supti, Sahu Shivani, Kaur Sajeev, Jain Suman
Faculty of Biological Sciences, University of Leeds, Woodhouse, Leeds, UK.
Institute of Microbial Technology, Chandigarh, India.
Ann Neurosci. 2020 Apr;27(2):49-56. doi: 10.1177/0972753120950072. Epub 2020 Oct 7.
Magnetic field (MF) stimulation has the potential to reduce secondary damage and promote functional recovery after neural tissue injury. The study aimed to observe the effect of very low intensity (17.96µT) MF on general body condition, secondary damage, pain status, and locomotion.
We exposed rats to MF (2 h/day × 3 weeks) after 6.25 mm contusion spinal injury. Locomotor behavior was evaluated by BBB score, pain assessment was done by recording threshold for tail flick, expression of voltage-gated calcium channels and extent of secondary damage in the spinal cord was assessed by immunofluorescence and Cresyl violet staining, respectively.
A significant ( ≤ .001) improvement in bladder function as well as BBB score was observed after MF exposure in comparison with sham and SCI over the observation period of 3 weeks. SCI group showed an increase in the threshold for vocalization after discharge, which decreased following MF exposure. Cresyl violet staining showed significantly higher tissue sparing (73%) at the epicenter after MF exposure when compared to SCI group. This was accompanied with a significant decrease in calcium channel expression in MF group as compared to SCI.
The results suggest facilitation of sensory-motor recovery after MF exposure, which could be due to attenuation of secondary damage and calcium-mediated excitotoxicity in a mild contusion rat model of SCI.
磁场(MF)刺激具有减少神经组织损伤后继发性损伤并促进功能恢复的潜力。本研究旨在观察极低强度(17.96µT)MF对大鼠整体身体状况、继发性损伤、疼痛状态和运动能力的影响。
在大鼠脊髓受到6.25mm挫伤后,将其暴露于MF(每天2小时×3周)。通过BBB评分评估运动行为,通过记录甩尾阈值进行疼痛评估,分别通过免疫荧光和甲酚紫染色评估脊髓中电压门控钙通道的表达和继发性损伤程度。
与假手术组和脊髓损伤组相比,在3周的观察期内,暴露于MF后的大鼠膀胱功能以及BBB评分有显著(≤.001)改善。脊髓损伤组在放电后发声阈值增加,而在暴露于MF后降低。与脊髓损伤组相比,甲酚紫染色显示暴露于MF后震中处的组织保留率显著更高(73%)。与脊髓损伤组相比,MF组钙通道表达显著降低。
结果表明,在轻度挫伤性脊髓损伤大鼠模型中,暴露于MF后感觉运动功能恢复得到促进,这可能是由于继发性损伤和钙介导的兴奋性毒性减弱所致。