Kim Min Sun, Koo Ho, Han Sang Who, Paulus Walter, Nitsche Michael A, Kim Yun-Hee, Yoon Jin A, Shin Yong-Il
Department of Physiology, Wonkwang University College of Medicine, Iksan, South Korea.
Department of Clinical Neurophysiology, University Medical Center, Georg-August-University, Goettingen, Germany.
Restor Neurol Neurosci. 2017;35(2):137-146. doi: 10.3233/RNN-160689.
Anodal transcranial direct current stimulation (A-tDCS) induces a long-lasting increase in cortical excitability that can increase gene transcription in the brain.
The purpose of this study was to evaluate the expression of genes related to activity-dependent neuronal plasticity in the sensorimotor cortex and hippocampus of young Sprague-Dawley rats following A-tDCS.
We applied A-tDCS over the right sensorimotor cortex epicranially with a circular electrode (3 mm diameter) at 250 μA for 20 min per day for 7 consecutive days. Levels of mRNA for brain-derived neurotrophic factor (BDNF), cAMP response element-binding protein (CREB), synapsin I, Ca2+/calmodulin-dependent protein kinase II (CaMKII), activity-regulated cytoskeleton-associated protein (Arc), and c-Fos were analyzed using SYBR Green quantitative real-time polymerase chain reaction (PCR).
We found that 7 days of unilateral A-tDCS resulted in significant increases in transcription of all plasticity-related genes tested in the ipsilateral cortex. Daily A-tDCS also resulted in a significant increase in c-Fos mRNA in the ipsilateral hippocampus.
These results indicate that altered expression of plasticity-associated genes in the cortex and hippocampus is a molecular substrate of A-tDCS-induced neural plasticity.
阳极经颅直流电刺激（A-tDCS）可使皮质兴奋性长期增强，进而增加大脑中的基因转录。
本研究旨在评估年轻的斯普拉格-道利大鼠在接受A-tDCS后，其感觉运动皮层和海马体中与活动依赖性神经元可塑性相关基因的表达情况。
我们使用圆形电极（直径3毫米），以250微安的电流，每天在右侧感觉运动皮层颅骨表面进行A-tDCS刺激，每次20分钟，连续进行7天。采用SYBR Green定量实时聚合酶链反应（PCR）分析脑源性神经营养因子（BDNF）、环磷酸腺苷反应元件结合蛋白（CREB）、突触素I、Ca2+/钙调蛋白依赖性蛋白激酶II（CaMKII）、活动调节细胞骨架相关蛋白（Arc）和c-Fos的mRNA水平。
我们发现，连续7天的单侧A-tDCS导致同侧皮层中所有测试的可塑性相关基因的转录显著增加。每日A-tDCS还导致同侧海马体中c-Fos mRNA显著增加。
这些结果表明，皮层和海马体中可塑性相关基因表达的改变是A-tDCS诱导神经可塑性的分子基础。
