1 Core Laboratory of Neuroscience, Office of R&D, Taipei Medical University, Taipei, Taiwan.
2 Translational Laboratory, Department of Medical Research, Taipei Medical University Hospital, Taipei, Taiwan.
J Neurotrauma. 2019 Apr 1;36(7):1054-1059. doi: 10.1089/neu.2018.5949. Epub 2018 Nov 17.
Mild traumatic brain injury (mTBI) constitutes 75 ∼ 90% of all TBI cases and causes various physical, cognitive, emotional, and other psychological symptoms. Nogo receptor 1 (NgR1) is a regulator of structural brain plasticity during development and in adulthood. Here, we used mice that, in the absence of doxycycline, overexpress NgR1 in forebrain neurons (MemoFlex) to determine the role of NgR1 in recovery from mTBI with respect to balance, cognition, memory, and emotion. We compared wild-type (WT), MemoFlex, and MemoFlex + doxycycline mice to the same three groups subjected to mTBI. mTBI was induced by a controlled 30-g weight drop. We found that inability to downregulate NgR1 significantly impairs recovery from mTBI-induced impairments. When the NgR1 transgene was turned off, recovery was similar to that of WT mice. The results suggest that the ability to regulate NgR1 signaling is needed for optimal recovery of motor coordination and balance, spatial memory, cognition, and emotional functions after mTBI.
轻度创伤性脑损伤（mTBI）占所有 TBI 病例的 75%∼90%，并导致各种身体、认知、情绪和其他心理症状。Nogo 受体 1（NgR1）是发育过程中和成年期大脑结构可塑性的调节剂。在这里，我们使用了在缺乏强力霉素的情况下在前脑神经元中过表达 NgR1 的小鼠（MemoFlex），以确定 NgR1 在 mTBI 恢复方面的作用，包括平衡、认知、记忆和情绪。我们将野生型（WT）、MemoFlex 和 MemoFlex +强力霉素小鼠与同样的三组接受 mTBI 的小鼠进行了比较。mTBI 通过受控的 30g 重量下降来诱导。我们发现，无法下调 NgR1 会显著损害 mTBI 引起的损伤的恢复。当 NgR1 转基因关闭时，恢复情况与 WT 小鼠相似。结果表明，调节 NgR1 信号的能力是 mTBI 后运动协调和平衡、空间记忆、认知和情绪功能恢复的最佳需要。
