Expression of S100A6 in Rat Hippocampus after Traumatic Brain Injury Due to Lateral Head Acceleration
by
Bo Fang 1,†, Ming Liang 1,†, Guitao Yang 2,†, Yuqin Ye 1, Hongyu Xu 1, Xiaosheng He 1,* and Jason H. Huang 3
Bo Fang 1,†, Ming Liang 1,†, Guitao Yang 2,†, Yuqin Ye 1, Hongyu Xu 1, Xiaosheng He 1,* and Jason H. Huang 3
1
Department of Neurosurgery, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China
2
Department of Medical, Teaching and Research Administration, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China
3
Department of Neurosurgery, University of Rochester, Rochester, NY 14642, USA
*
Author to whom correspondence should be addressed.
†
These authors contributed equally to this work.
Int. J. Mol. Sci. 2014, 15(4), 6378-6390; https://doi.org/10.3390/ijms15046378
Received: 15 December 2013 / Revised: 25 March 2014 / Accepted: 31 March 2014 / Published: 15 April 2014
(This article belongs to the Special Issue Neurological Injuries’ Monitoring, Tracking and Treatment)
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.
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Keywords:
S100A6; hippocampus; cognitive deficits; traumatic brain injury (TBI); rats
This is an open access article distributed under the Creative Commons Attribution License
MDPI and ACS Style
Fang, B.; Liang, M.; Yang, G.; Ye, Y.; Xu, H.; He, X.; Huang, J.H. Expression of S100A6 in Rat Hippocampus after Traumatic Brain Injury Due to Lateral Head Acceleration. Int. J. Mol. Sci. 2014, 15, 6378-6390.
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