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江 山,李娅娜,王会会,曹 岚,王一鸣,李 玲.低频经颅磁刺激对缺血缺氧脑损伤大鼠学习记忆及体外培养缺血缺氧神经元谷氨酸释放的影响[J].中国康复医学杂志,2019,(12):1397~1402
低频经颅磁刺激对缺血缺氧脑损伤大鼠学习记忆及体外培养缺血缺氧神经元谷氨酸释放的影响    点此下载全文
江 山  李娅娜  王会会  曹 岚  王一鸣  李 玲
解放军总医院第四医学中心,北京市,100048
基金项目:国家自然科学基金(81472168);北京市自然科学基金(7172208)
DOI:
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摘要:
      摘要 目的:观察低频经颅磁刺激(TMS)对缺血缺氧脑损伤(HIBI)大鼠学习记忆能力的影响,同时探讨低频TMS对体外培养的缺血缺氧(HI)大鼠神经元谷氨酸释放的影响。 方法:选用成年SD大鼠,制作缺血缺氧模型,将模型大鼠分为如下三组:HIBI组,TMS+HIBI组以及正常对照组。采用水迷宫来评估大鼠的学习记忆能力。与此同时,我们还体外培养大鼠海马区神经元,同样将其分为HI组、TMS+HI组以及正常对照组。采用氧气葡萄糖剥夺法制作细胞缺血缺氧模型,测定细胞外液谷氨酸及乳酸脱氢酶(LDH)浓度(与神经元损伤呈正相关),同时观察细胞存活率。 结果:①HIBI后,WM结果显示大鼠的学习记忆能力受损,与正常对照组相比较,有显著差异(P<0.05)。②经过TMS刺激14d后,TMS+HIBI组大鼠的学习记忆能力高于HIBI组(P<0.05)。③HI刺激后,体外培养的神经元细胞外液谷氨酸及LDH浓度升高,显著高于正常对照组(P<0.05),而神经元存活率则显著下降,低于正常对照组(P<0.05)。④TMS+HI组神经元细胞外液谷氨酸和LDH浓度低于HI组(P<0.05),神经元存活率也显著上升,高于HI组(P<0.05)。 结论:①HIBI后,大鼠学习记忆能力显著下降,而低频TMS 可以显著改善HIBI大鼠的认知功能;②HI诱导体外培养的神经元损伤,谷氨酸释放增加,细胞存活率降低,而低频TMS可以抑制HI诱导的神经元损伤以及谷氨酸释放,减轻谷氨酸毒性作用,同时增加神经元存活率。这可能与低频TMS改善学习记忆能力有关,这为缺血缺氧脑损伤的治疗提供了新的思路。
关键词:低频经颅磁刺激  缺血缺氧脑损伤  学习记忆能力  谷氨酸  乳酸脱氢酶
The effect of low-frequency transcranial magnetic stimulation on the learning and memory ability of rats with hypoxia-ischemic brain injury and glutamate release by cultured neuron after hypoxia-ischemia    Download Fulltext
The First Affiliated Hospital, Chinese PLA General Hospital,Beijing,100048
Fund Project:
Abstract:
      Abstract Objective:To investigate the effect of low-frequency transcranial magnetic stimulation(TMS) on the learning and memory ability of rats with hypoxia-ischemic brain injury(HIBI) and glutamate release by cultured neuron after hypoxia-ischemia(HI). Method:SD rats were randomly divided into three groups(n=6): HIBI group, HIBI+TMS group and control group. Morris water maze was used to evaluate the learning and memory capacity. Furthermore, we also cultured the hippocampal neuron of rats in vitro and the HI model was made by oxygen glucose deprivation(OGD). We detected the glutamate and lactate dehydrogenase (LDH) levels in extracellular fluid. And at the same time cell survival rate was also observed. Result:①Learning and memory capacity of rats significantly decreased after HIBI(P<0.05, vs control group. ②After TMS treatment for 14 days, the learning and memory capacity significantly increased for HIBI rats(P<0.05, HIBI+TMS group vs HIBI group). ③For cultured neurons after HI, the levels of glutamate and LDH in extracellular fluid increased, but accompanied by the decrease of cell survival rate(P<0.05, vs control group). ④As in vivo, the levels of glutamate and LDH exhibited the decreased trend and the cell survival rate also increased after TMS treatment(P<0.05, TMS+HI group vs HI group). Conclusion:①HIBI decreases the learning and memory ability, while TMS could alleviate this effect. ②HI increases the release of glutamate and decreases the cell survival rate, which could be inhibited by TMS. Thus, the present study makes a novel idea for the treatment of cognitive disorders after HIBI.
Keywords:low-frequency transcranial magnetic stimulation  hypoxia-ischemic brain injury  learning and memory capacity  glutamate  lactate dehydrogenase
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