Citation

Madathil SK, Deng-Bryant Y, Wilfred BS, Leung LY, Gilsdorf JS, Shear DA. J. Trauma Acute Care Surg. 2017; ePub(ePub): ePub.

Affiliation

1 Brain Trauma Neuroprotection and Neurorestoration Branch, Center for Military Psychiatry and Neuroscience, Walter Reed Army Institute of Research (WRAIR), 503 Robert Grant Ave, Silver Spring, 20910, MD, USA.

Copyright

(Copyright © 2017, Lippincott Williams and Wilkins)

DOI

10.1097/TA.0000000000001471

PMID

28383475

Abstract

BACKGROUND: Brain derived neurotrophic factor (BDNF) and Insulin-like growth factor-1 (IGF-1) are essential for neuroplasticity and neuronal survival. Despite the importance of these endogenous factors in mediating post-traumatic recovery, little is known about their response after penetrating type traumatic brain injury (TBI). The objective of this study was to quantify the expression levels BDNF and IGF-1, two well-known neuroplasticity mediators, following penetrating ballistic-like brain injury (PBBI).

METHODS: Rats were randomly assigned to receive unilateral sham or PBBI injuries. Using ELISA and immunohistochemistry we performed a comprehensive evaluation of BDNF and IGF-1 expression at acute (1h, 6h, 1d) and sub-acute (2d, 3d, 7d and 14d) time points following injury.

RESULTS: BDNF and IGF-1 expression was transiently upregulated in both cortex and hippocampus following PBBI. While BDNF levels increased at acute time points, IGF-1 expression peaked at 3d in cortical homogenates. Although there was loss of staining in cells bordering the cavity, increased BDNF and IGF-1 immunoreactivity was observed in scattered neurons away from the contusion site. Glial upregulation of both growth factors were observed at early time points in the hippocampus.

CONCLUSION: Our findings demonstrate that PBBI results in a brief upregulation of BDNF and IGF-1 during early post-traumatic period, providing critical information for interventions aiming to enhance neuronal survival and brain plasticity.

Language: en