Transient versus prolonged hyperlocomotion following lateral fluid percussion injury in mongolian gerbils
Article first published online: 5 JAN 2006
Copyright © 2006 Wiley-Liss, Inc.
Journal of Neuroscience Research
Volume 83, Issue 2, pages 292–300, 1 February 2006
How to Cite
Li, S., Kuroiwa, T., Katsumata, N., Ishibashi, S., Sun, L. Y., Endo, S. and Ohno, K. (2006), Transient versus prolonged hyperlocomotion following lateral fluid percussion injury in mongolian gerbils. J. Neurosci. Res., 83: 292–300. doi: 10.1002/jnr.20720
- Issue published online: 17 JAN 2006
- Article first published online: 5 JAN 2006
- Manuscript Accepted: 12 OCT 2005
- Manuscript Revised: 11 OCT 2005
- Manuscript Received: 8 SEP 2005
- cognitive dysfunction;
- traumatic brain injury;
- white matter rarefaction
Posttraumatic hyperactivity is a neurobehavioral symptom commonly seen in patients after traumatic brain injury (TBI). No useful animal model has yet been established for evaluation of this important symptom. We induced either mild (MILD, 0.7–0.9 atm) or moderate (MOD, 1.3–1.6 atm) lateral fluid percussion injury (LFPI) in Mongolian gerbils. Open-field and T-maze tests were used during a 7-day period after the trauma. All animals were perfusion fixed for histopathological examinations. Transient locomotor hyperactivity was found with a peak at 6 hr after injury in the MILD animals, whereas MOD animals showed prolonged and severe hyperlocomotion throughout the 7-day posttrauma period (P < 0.0001). Interestingly, the temporal profile of the posttraumatic hyperactivity was similar to that of the working memory deficit in both injury groups. Histological examination revealed significant neural tissue damages, including cortical necrosis, white matter rarefaction, and neuronal loss in the hippocampus in the ipsilateral hemisphere of the MOD animals, vs. only negligible changes in the MILD animals. Correlation analysis revealed that the volume of white matter lesions was significantly correlated with both posttraumatic hyperactivity (r = 0.591, P < 0.01) and working memory deficit (r = −0.859, P < 0.0001). Taken together, our findings confirm the successful reproduction of posttraumatic hyperactivity following experimental TBI. The posttraumatic hyperlocomotion probably shared pathomechanisms common to those of cognitive dysfunction caused by LFPI, supporting the speculation from previous studies that some neurobehavioral abnormities intimately correlate with TBI-induced cognitive dysfunction. Histopathologically, significant involvement of white matter damage in the posttraumatic functional deficits was indicated. © 2006 Wiley-Liss, Inc.