Preprint Article Version 1 This version is not peer-reviewed

Neurodegeneration and Sensorimotor Deficits in the Mouse Model of Traumatic Brain Injury

Version 1 : Received: 27 December 2017 / Approved: 28 December 2017 / Online: 28 December 2017 (08:58:32 CET)

A peer-reviewed article of this Preprint also exists.

Bhowmick, S.; D‘Mello, V.; Ponery, N.; Abdul-Muneer, P.M. Neurodegeneration and Sensorimotor Deficits in the Mouse Model of Traumatic Brain Injury. Brain Sci. 2018, 8, 11. Bhowmick, S.; D‘Mello, V.; Ponery, N.; Abdul-Muneer, P.M. Neurodegeneration and Sensorimotor Deficits in the Mouse Model of Traumatic Brain Injury. Brain Sci. 2018, 8, 11.

Journal reference: Brain Sci. 2018, 8, 11
DOI: 10.3390/brainsci8010011

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 TUNEL staining and PARP and annexin V western blotting. We correlated the neurodegeneration with sensorimotor deficits by conducting the animal behavioral tests including grid walk, balance beam, inverted screen test, and climb test. Our study demonstrated that the excess cell death or neurodegeneration correlated with the neuronal dysfunction and sensorimotor impairments associated with TBI.

Subject Areas

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

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