Histological and Behavioral Evaluation after Traumatic Brain Injury in Mice: A Ten Months Follow-Up Study
| Autor: | Kristin Simon, Claire Leconte, Federica Lentini, Catherine Marchand-Leroux, Michel Plotkine, Raymond Mongeau, Toufik Taib, Chahid Ouaazizi, Angelo Cho, Valérie C. Besson, Chiara Benedetto |
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| Rok vydání: | 2020 |
| Předmět: |
Male
030506 rehabilitation medicine.medical_specialty Time Factors Traumatic brain injury Context (language use) Motor incoordination Mice 03 medical and health sciences 0302 clinical medicine Physical medicine and rehabilitation Brain Injuries Traumatic medicine Animals Maze Learning business.industry Cognitive flexibility Follow up studies Brain Cognition medicine.disease Exploratory Behavior Neurology (clinical) 0305 other medical science business 030217 neurology & neurosurgery Follow-Up Studies |
| Zdroj: | Journal of Neurotrauma. 37:1342-1357 |
| ISSN: | 1557-9042 0897-7151 |
| Popis: | Traumatic brain injury (TBI) is a chronic pathology, inducing long-term deficits that remain understudied in pre-clinical studies. In this context, exploration, anxiety-like behavior, cognitive flexibility, and motor coordination were assessed until 5 and 10 months after an experimental TBI in the adult mouse, using two cohorts. In order to differentiate age, surgery, and remote gray and white matter lesions, three groups (unoperated, sham-operated, and TBI) were studied. TBI induced delayed motor coordination deficits at the pole test, 4.5 months after injury, that could be explained by gray and white matter damages in ipsilateral nigrostriatal structures (striatum, internal capsule) that were spreading to new structures between cohorts, at 5 versus 10 months after the injury. Further, TBI induced an enhanced exploratory behavior during stressful situations (active phase during actimetry test, object exploration in an open field), risk-taking behaviors in the elevated plus maze 5 months after injury, and a cognitive inflexibility in the Barnes maze that persisted until 9 months after the injury. These behavioral modifications could be related to the white and gray matter lesions observed in ipsi- and contralateral limbic structures (amygdala, hilus/cornu ammonis 4, hypothalamus, external capsule, corpus callosum, and cingular cortex) that were spreading to new structures between cohorts, at 5 months versus 10 months after the injury. The present study corroborates clinical findings on TBI and provides a relevant rodent chronic model which could help in validating pharmacological strategies against the chronic consequences of TBI. |
| Databáze: | OpenAIRE |
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