经颅直流电刺激对实验性脑外伤模型运动和认知功能障碍的影响

Guven Akcay, Filiz Demirdogen, Tuba Gul, Ali Yilmaz, Dilcan Kotan, Esra Karakoc, Huseyin Emre Ozturk, Cagla Celik, Haydar Celik, Yavuz Erdem
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引用次数: 0

摘要

目的:研究经颅直流电刺激(tDCS)对创伤性脑损伤(TBI)引起的谷氨酸和钙兴奋毒性以及运动和认知功能丧失的治疗和神经保护作用:将 40 只大鼠平均分为假组、TBI 组、tDCS + TBI + tDCS 组和 TBI + tDCS 组。从 1 米高处向大鼠头骨投掷 450 克重的铁块,诱发轻度 TBI。TDCS + TBI + tDCS 组在诱发 TBI 前 5 天开始预防性地给予 30 分钟 1 毫安的刺激,持续 7 天。在 TBI + tDCS 组中,在 TBI 发生 2 小时后的第 1 天和第 2 天对大鼠进行 tDCS 刺激(1 毫安,30 分钟)。认知和运动功能通过新物体识别和开阔地测试进行评估。用酶联免疫吸附法测定了海马中钙、谷氨酸和 N-甲基-D-天冬氨酸受体 1(NMDAR1)的水平:结果:虽然与假体相比,创伤性脑损伤组的运动和认知功能大幅下降,但治疗组的运动和认知功能有所改善(P < 0.05)。创伤性脑损伤组的钙离子、谷氨酸和 NMDAR1 水平明显高于假体组(p < 0.001)。然而,tDCS + TBI + tDCS 组和 TBI + tDCS 组的钙离子、谷氨酸和 NMDAR1 水平大大低于 TBI 组(p < 0.05)。尤其是 tDCS + TBI + tDCS 组的变化高于 TBI + tDCS 组:结论:在发生 TBI 之前应用 tDCS 可以改善运动和认知功能障碍。结论:在创伤性脑损伤发生前应用 TDCS 可改善运动和认知功能障碍,通过调节钙和谷氨酸水平减少兴奋性毒性,从而起到神经保护和治疗作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effects of Transcranial Direct Current Stimulation on Motor and Cognitive Dysfunction in an Experimental Traumatic Brain Injury Model.

Aim: To investigate the therapeutic and neuroprotective effects of transcranial direct current stimulation (tDCS) application on the traumatic brain injury (TBI)-induced glutamate and calcium excitotoxicity and loss of motor and cognitive functions.

Material and methods: Forty rats were equally divided in the sham, TBI, tDCS + TBI + tDCS, and TBI + tDCS groups. Mild TBI was induced by dropping a 450-g iron weight from a height of 1 m onto the skull of the rats. The tDCS + TBI + tDCS group was prophylactically administered 1 mA stimulation for 30 min for 7 days starting 5 days before inducing TBI. In the TBI + tDCS group, tDCS (1 mA for 30 min) was administered 2 h after TBI, on days 1 and 2. Cognitive and locomotor functions were assessed using the novel object recognition and open field tests. The calcium, glutamate, and N-methyl-D-aspartate receptor 1 (NMDAR1) levels in the hippocampus were measured using enzyme-linked immunosorbent assay.

Results: Although the motor and cognitive functions were substantially reduced in the TBI group when compared with the sham, they improved in the treatment groups (p < 0.05). The calcium, glutamate, and NMDAR1 levels were considerably higher in the TBI group than in the sham (p < 0.001). However, they were considerably lower in the tDCS + TBI + tDCS and TBI + tDCS groups than in the TBI groups (p < 0.05). In particular, the change in the tDCS + TBI + tDCS group was higher than that in the TBI + tDCS group.

Conclusion: Application of tDCS before the development of TBI improved motor and cognitive dysfunction. It demonstrated a neuroprotective and therapeutic effect by reducing the excitotoxicity via the regulation of calcium and glutamate levels.

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