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Int J Mol Sci. 2014 Apr 15;15(4):6378-90. doi: 10.3390/ijms15046378.

Expression of S100A6 in rat hippocampus after traumatic brain injury due to lateral head acceleration.

Author information

  • 1Department of Neurosurgery, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China. happyfangbo@gmail.com.
  • 2Department of Neurosurgery, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China. liangming777@163.com.
  • 3Department of Medical, Teaching and Research Administration, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China. guitaoy@hotmail.com.
  • 4Department of Neurosurgery, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China. chinayeyuqin@163.com.
  • 5Department of Neurosurgery, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China. xuhy@fmmu.edu.cn.
  • 6Department of Neurosurgery, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China. hexiaos@fmmu.edu.cn.
  • 7Department of Neurosurgery, University of Rochester, Rochester, NY 14642, USA. jason_huang@urmc.rochester.edu.

Abstract

In a rat model of traumatic brain injury (TBI), we investigated changes in cognitive function and S100A6 expression in the hippocampus. TBI-associated changes in this protein have not previously been reported. Rat S100A6 was studied via immunohistochemical staining, Western blot, and reverse transcription-polymerase chain reaction (RT-PCR) after either lateral head acceleration or sham. Reduced levels of S100A6 protein and mRNA were observed 1 h after TBI, followed by gradual increases over 6, 12, 24, and 72 h, and then a return to sham level at 14 day. Morris water maze (MWM) test was used to evaluate animal spatial cognition. TBI- and sham-rats showed an apparent learning curve, expressed as escape latency. Although TBI-rats displayed a relatively poorer cognitive ability than sham-rats, the disparity was not significant early post-injury. Marked cognitive deficits in TBI-rats were observed at 72 h post-injury compared with sham animals. TBI-rats showed decreased times in platform crossing in the daily MWM test; the performance at 72 h post-injury was the worst. In conclusion, a reduction in S100A6 may be one of the early events that lead to secondary cognitive decline after TBI, and its subsequent elevation is tightly linked with cognitive improvement. S100A6 may play important roles in neuronal degeneration and regeneration in TBI.

PMID:
24739809
[PubMed - in process]
PMCID:
PMC4013634
Free PMC Article

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