Traumatic Brain Injury in Young Rats Leads to Progressive Behavioral Deficits Coincident with Altered Tissue Properties in Adulthood
| Autor: | Joel E. Kamper, Andre Obenaus, Viorela Pop, Richard E. Hartman, David O. Ajao, Stephen Ashwal, Arash Adami, Roman Vlkolinsky, Emil Rudobeck, Lei Huang, Jérôme Badaut |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2012 |
| Předmět: |
Male
Traumatic brain injury Posterior parietal cortex Poison control White matter Lesion Rats Sprague-Dawley Myelin medicine Animals Behavior Animal Mental Disorders Brain Original Articles medicine.disease Immunohistochemistry Magnetic Resonance Imaging Rats Electrophysiology Disease Models Animal medicine.anatomical_structure Brain Injuries Brain size Neurology (clinical) medicine.symptom Psychology Neuroscience |
| Popis: | 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 post-natal day (P) 17 to evaluate behavioral alterations, injury volume, and morphological and molecular changes in gray and white matter, with accompanying measures of electrophysiological function. At 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, as well as 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 dysfunction, occurring in parallel with the delayed development and persistence of behavioral deficits, thus modeling clinical and longitudinal TBI observations. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|