Citation

Ajao D, Pop V, Kamper J, Adami A, Rudobeck E, Huang L, Vlkolinsky R, Hartman R, Ashwal S, Obenaus A, Badaut J. J. Neurotrauma 2012; 29(11): 2060-2074.

Affiliation

Loma Linda University, Physiology, Loma Linda, California, United States; dajao@llu.edu.

Copyright

(Copyright © 2012, Mary Ann Liebert Publishers)

DOI

10.1089/neu.2011.1883

PMID

22697253

Abstract

Traumatic brain injury (TBI) affects many infants and children and results in enduring motor and cognitive impairments with accompanying changes in white matter tracts, yet few experimental studies in rodent juvenile models of TBI (jTBI) have examined the timeline and nature of these deficits, histologically and functionally. We used a single controlled cortical impact (CCI) injury to the parietal cortex of rats at postnatal day (P) 17 to evaluate behavioral alterations, injury volume, morphological and molecular changes in gray and white matter with accompanying measures of electrophysiological function. After 60 days post-injury (dpi), we found that jTBI animals displayed behavioral deficits in foot-fault and rotarod tests along with a left turn bias throughout their early developmental stages and into adulthood. In addition, anxiety-like behaviors on the zero maze emerged in jTBI animals at 60 dpi. The final lesion constituted only ~3% of brain volume and morphological tissue changes were evaluated using MRI, and immunohistochemistry for neuronal nuclei (NeuN), myelin basic protein (MBP), neurofilament-200 (NF200), and oligodendrocytes (CNPase). White matter morphological changes were associated with a global increase in MBP immunostaining and reduced compound action potential amplitudes at 60 dpi. These results suggest that brain injury early in life can induce long-term white matter dysfunctions occurring in parallel with the delayed development and persistence of behavioral deficits, thus modeling clinical and longitudinal TBI observations.

Language: en