Traumatic Brain Injury elevates catecholamine biosynthesis in the rat adrenal medulla

Abstract

Traumatic Brain Injury (TBI), produces major health problems impacting the lives of people. TBI disrupts noradrenergic pathways leading to autonomic dysfunction but the nature of this disruption is unknown. Following TBI, we assesed selective biochemical markers for autonomic function in adult female Sprague Dawley rats. Closed head TBI was produced using Marmarou protocol (450 g/1.25m weight drop). Sympathetic nervous system (SNS) activation of the adrenal medullae (AM) was evaluated at 3 months following TBI by assessing the expression of catecholamine biosynthesizing enzymes, tyrosine hydroxylase (TH) and dopamine-β hydroxylase (DβH), along with Neuropeptide Y (NPY). DβH expression increased by 57% (P<0.05), but TH expression was unchanged following TBI. NPY expression was significantly elevated by 60% (P<0.05) in TBI compared with age-matched controls. NPY is synthesized and co-realesed with catecholamines in the AM and NPY expression correlates with catecholamine biosynthesis. Collectively, the increased DβH and NPY expression in the rat AM suggest that closed head TBI results in increased sympathoexcitation. Such effects may be one of the important factors contributing to autonomic dysfunction following TBI. Supported by Department of Veteran Affairs; Rehabilitation R&D, GRECC, Medical Research Services, National Institute of Aging, and American Heart Association.