Neurodegeneration and Sensorimotor Deficits in the Mouse Model of Traumatic Brain Injury
Laboratory of CNS Injury and Repair, Neuroscience Institute, JFK Medical Center, 65 James St, Edison, NJ 08820, USA
Author to whom correspondence should be addressed.
Brain Sci. 2018, 8(1), 11; https://doi.org/10.3390/brainsci8010011
Received: 19 November 2017 / Revised: 27 December 2017 / Accepted: 4 January 2018 / Published: 6 January 2018
(This article belongs to the Special Issue Novel Mechanisms and Strategies for Neural Repair)
Traumatic brain injury (TBI) can result in persistent sensorimotor and cognitive deficits, which occur through a cascade of deleterious pathophysiological events over time. In this study, we investigated the hypothesis that neurodegeneration caused by TBI leads to impairments in sensorimotor function. TBI induces the activation of the caspase-3 enzyme, which triggers cell apoptosis in an in vivo model of fluid percussion injury (FPI). We analyzed caspase-3 mediated apoptosis by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining and poly (ADP-ribose) polymerase (PARP) and annexin V western blotting. We correlated the neurodegeneration with sensorimotor deficits by conducting the animal behavioral tests including grid walk, balance beam, the inverted screen test, and the climb test. Our study demonstrated that the excess cell death or neurodegeneration correlated with the neuronal dysfunction and sensorimotor impairments associated with TBI.