Citation

Lai JH, Karlsson TE, Wu JC, Huang CZ, Chen YH, Kang SJ, Brodin ATS, Hoffer BJ, Olson L, Chiang YH, Chen KY. J. Neurotrauma 2019; 36(7): 1054-1059.

Affiliation

Taipei Medical University, Graduate Institute of Neural Regenerative Medicine , 250, Wu Xing Street , Taipei, Taiwan , 110 ; kychen08@tmu.edu.tw.

Copyright

(Copyright © 2019, Mary Ann Liebert Publishers)

DOI

10.1089/neu.2018.5949

PMID

30226403

Abstract

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 wildtype (WT), MemoFlex and MemoFlex + doxycycline mice to the same three groups subjected to mTBI. mTBI was induced by a controlled 30g weight drop. We found that inability to down-regulate 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 ability to regulate NgR1 signaling is needed for optimal recovery of motor coordination and balance, spatial memory, cognition and emotional functions after mTBI.

Language: en

Keywords

COGNITIVE FUNCTION; Nogo Receptors; TRAUMATIC BRAIN INJURY