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Introduction: Traumatic Brain Injury (TBI) produces major health problems impacting the lives of both military and civilian personnel. TBI disrupts autonomic function but the nature of this disruption is unknown. Following blast brain injury, we assessed selective biochemical markers for autonomic function in adult male Sprague Dawley rats. Methods: Rats were subjected to head-directed overpressure blast injury (OBI) of 358 kPa magnitude at the target. At the same time for sham controls, rats were anesthetized as the previous group but instead of OBI were exposed just to noise being placed at ~ 2 m distance from the shock tube nozzle. Sympathetic nervous system activation of nucleus tractus solitaries and in the hypothalamus was evaluated at 6 hours following blast injury by assessing the expression of catecholamine biosynthesizing enzyme, tyrosine hydroxylase (TH) in the nucleus tractus solitaries and NADPH oxidase activity, a marker of oxidative stress,in the hypothalamus. Results: Following OBI there was a significant elevation in TH protein expression by 49% compared with control (P<0.05). In addition, NADPH oxidase activity was significantly increased by 36% following OBI (P<0.05). Conclusions: Collectively, the increased catecholamine biosynthesis in nucleus tractus solitaries and oxidative stress in the hypotalamus suggest that OBI results in increased sympathoexcitation in the rat brain. Such effects may be one important factor contributing to autonomic dysfunction following OBI. Acknowledgements: Supported by Department of Veteran Affairs; Rehabilitation R&D, GRECC, Medical Research Services, Banyan Biomarkers Inc, University of Florida Brain Institute, NIA, and AHA

Publication Title

Journal of Neurotrauma




Mary Ann Liebert Inc






This is a copy of an article published in the Journal of Neurotrauma © 2012; the Journal of Neurotrauma is available online at:

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