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作 者:李勇志 吴雨 马梦启 汪际慧[1] 董雪芬[1] 欧阳玮[1] LI Yong-Zhi;WU Yu;MA Meng-Qi;WANG Ji-Hui;DONG Xue-Fen;OUYANG Wei(College of Physical Education and Health Sciences,Zhejiang Normal University,Jinhua 321004,China)
机构地区:[1]浙江师范大学体育与健康科学学院,金华321004
出 处:《生理学报》2024年第1期12-32,共21页Acta Physiologica Sinica
基 金:supported by the Natural Science Foundation of Zhejiang Province(No.LY20H150001);the Key Social Development Foundation of Jinhua Municipality(No.2020-3-071)。
摘 要:本研究旨在探讨中度创伤性脑损伤(traumatic brain injury,TBI)后C57BL/6J小鼠海马CA1与内嗅皮层(medial entorhinal cortex,MEC)功能相互作用变化,以及综合性运动(comprehensive exercise,CE)可能产生的有益效果。TBI后,将两个微电极植入CA1和MEC进行细胞外记录,我们发现CA1和MEC部位神经元放电明显同步,特别是在100 Hz范围内,放电同步峰值在20~30 Hz;TBI导致20~40 Hz频段放电相关系数显著降低(P<0.001);在20~40 Hz和56~100 Hz范围内,所有组小鼠在MEC部位平均功率密度(power spectral density,PSD)均高于CA1部位的PSD;在CA1和MEC,TBI可导致20~40 Hz或56~100 Hz平均PSD(P<0.001或P<0.01)显著性及同步性增加;TBI小鼠表现出更加多样化的神经元放电模式,且簇发放电频率、簇发放电持续时间、簇发放电内放电间隔和簇发放电间隔均增加;损伤小鼠也表现出神经功能、睡眠、步态和工作记忆障碍;而CE可促进TBI小鼠上述电生理特征和功能障碍的恢复。以上结果提示,CE对TBI功能障碍的有益影响可能部分归因于CA1和MEC之间神经网络相互作用的改善。The present study aimed to investigate the alterations in functional interaction between hippocampal CA1 and medial entorhinal cortex(MEC)after moderate traumatic brain injury(TBI)in C57BL/6J mice,and the possible beneficial effects of comprehensive exercise(CE).Following TBI,two microelectrodes were implanted into CA1 and MEC for extracellular recording.We found a clear synchronization of neuronal firing in CA1 and MEC,particularly within 100 Hz and peaked at 20–30 Hz range.TBI induced a significant reduction(P<0.001)of the coherences of firing between 20–40 Hz frequency band.The mean power spectral densities(PSD)of all group mice in MEC were steadily larger than the values in CA1 in both 20–40 Hz and 56–100 Hz ranges.TBI induced significant and consistent increases of averaged 20–40 Hz or 56–100 Hz PSD(P<0.001 or P<0.01)in both CA1 and MEC.Injured mice displayed more varied firing patterns,and showed increased burst frequency(BF),burst duration(BD),inter-spike intervals(ISI)and inter-burst interval(IBI).Injured mice also showed worsened neurological function,sleep,gait performance,and working memory.CE facilitated the restoration of aforementioned electrophysiological characteristics and functional deficits in TBI mice.These results suggest that the beneficial effects of CE on TBI functional deficits may be partly attributed to improved neuronal network interaction between CA1 and MEC.
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