Neurological Research ( IF 1.9 ) Pub Date : 2021-08-16 , DOI: 10.1080/01616412.2021.1965427 Shih-Huang Tai, Liang-Chun Chao, Tung-Yi Huang, Che- Chao Chang, Sheng-Yang Huang, Tian-Shung Wu, E-Jian Lee
ABSTRACT
Objectives
Lithium exerts a broad neuroprotective effect on the brain. This study examined whether lithium exerts therapeutic effects on stroke by restoring neural connections at the ischemic core of cortices post brain insult.
Methods
We treated rats with lithium or vehicle (saline) every 24 h for the first 72 h, starting at the beginning of reperfusion after inducing middle cerebral artery occlusion (MCAO) in rats. Somatosensory evoked potential (SSEP) recording and behavioral testing were employed to evaluate the beneficial effects of lithium treatment. To examine the effects of lithium-induced neuroplasticity, we evaluated the dendritic morphology in cortex pyramidal cells and the primary neuronal cell culture that underwent brain insults and oxygen and glucose deprivation (OGD), respectively.
Results
The results demonstrated that rats subjected to MCAO had prolonged N1 latency and a decreased N1/P1 amplitude at the ipsilateral cortex. Four doses of lithium reduced the brain infarction volume and enhanced the SSEP amplitude. The results of neurobehavioral tests demonstrated that lithium treatment improved sensory function, as demonstrated by improved 28–point clinical scale scores. In vitro study results showed that lithium treatment increased the dendritic lengths and branches of cultured neurons and reversed the suppressive effects of OGD. The in vivo study results indicated that lithium treatment increased cortical spine density in various layers and resulted in the development of the dendritic structure in the contralateral hemisphere.
Conclusion
Our study confirmed that neuroplasticity in cortical neurons is crucial for lithium-induced brain function 50 recovery after brain ischemia.
中文翻译:
短期锂治疗通过增强皮质神经元的神经可塑性来保护大脑免受缺血再灌注损伤
摘要
目标
锂对大脑具有广泛的神经保护作用。本研究通过在脑损伤后恢复皮质缺血核心的神经连接来检查锂是否对中风产生治疗作用。
方法
我们在前 72 小时内每 24 小时用锂或载体(盐水)对大鼠进行一次治疗,从诱导大鼠大脑中动脉闭塞 (MCAO) 后开始再灌注开始。体感诱发电位 (SSEP) 记录和行为测试用于评估锂治疗的有益效果。为了检查锂诱导的神经可塑性的影响,我们分别评估了皮质锥体细胞和初级神经元细胞培养物中的树突形态,这些细胞培养物分别经历了脑损伤和氧气和葡萄糖剥夺 (OGD)。
结果
结果表明,接受 MCAO 的大鼠在同侧皮层具有延长的 N1 潜伏期和降低的 N1/P1 幅度。四剂锂减少了脑梗死体积并增强了 SSEP 幅度。神经行为测试的结果表明,锂治疗改善了感觉功能,改善了 28 分临床量表评分。体外研究结果表明,锂处理增加了培养神经元的树突长度和分支,并逆转了 OGD 的抑制作用。体内研究结果表明,锂处理增加了各层的皮质脊柱密度,并导致对侧半球树突结构的发展。
结论
我们的研究证实,皮质神经元的神经可塑性对于脑缺血后锂诱导的脑功能 50 恢复至关重要。