Citation

Bhowmick S, D'Mello V, Ponery N, Abdul-Muneer PM. Brain Sci. 2018; 8(1): e8010011.

Affiliation

Laboratory of CNS Injury and Repair, Neuroscience Institute, JFK Medical Center, 65 James St, Edison, NJ 08820, USA. mmuneer@jfkhealth.org.

Copyright

(Copyright © 2018, Switzerland Molecular Diversity Preservation International (MDPI) AG)

DOI

10.3390/brainsci8010011

PMID

29316623

Abstract

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.

Language: en

Keywords

apoptosis; fluid percussion injury; neurodegeneration; sensorimotor deficit; traumatic brain injury