Mild Fluid Percussion Injury in Mice Produces Evolving Selective Axonal Pathology and Cognitive Deficits Relevant to Human Brain Injury

• DOI: 10.1089/neu.2010.1288
• Publication Date: 2010-06-07T17:13:56Z
• Authors: Aisling Spain; Stephanie Daumas; Jonathan Lifshitz; Jonathan Rhodes; Peter J.D. Andrews; Karen Horsburgh; Jill H. Fowler
• Keywords: Diffuse axonal injury; Brain damage; Blast injury

Mild traumatic brain injury (TBI) accounts for up to 80% of clinical TBI and can result in cognitive impairment white matter damage that may develop persist over several years. Clinically relevant models mild investigation neurobiological changes the development therapeutic strategies are poorly developed. In this study we investigated temporal profile axonal somal contribute impairments a mouse model TBI. Neuronal perikaryal (hematoxylin eosin Fluoro-Jade C), myelin integrity (myelin basic protein myelin-associated glycoprotein), (amyloid precursor protein), were evaluated by immunohistochemistry at 4 h, 24 72 weeks, 6 weeks after lateral fluid percussion (0.9 atm; righting time 167 ± 15 sec). At 3 post-injury spatial reference learning memory tested Morris water maze (MWM). Levels neuronal cell bodies comparable brain-injured sham groups. Myelin was minimally altered following injury. Clear alterations observed various points Axonal localized cingulum h post-injury. post-injury, evident external capsule, seen dorsal thalamic nuclei. injured mice showed an impaired ability learn task, suggesting injury-induced search strategy learning. The evolving localization ongoing degeneration is concomitant with deficit