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Blast brain injury elevates catecholamine biosynthesis in the rat adrenal medulla
Author(s) -
Tümer Nihal,
Svetlov Stanislav,
Kirichenko Nataliya,
Whidden Melissa,
Erdos Benedek,
Prima Victor,
Sherman Alexandra,
Kobeissy Firas,
Yezierski Robert,
Vierck Charles Charles,
Wang Kevin
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1094.6
Subject(s) - tyrosine hydroxylase , catecholamine , neuropeptide y receptor , endocrinology , medicine , traumatic brain injury , dopamine , adrenal medulla , baroreflex , blood pressure , heart rate , neuropeptide , psychiatry , receptor
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 brain injury, we assesed selective biochemical markers for autonomic function in adult male Sprague Dawley rats. 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 the adrenal medullae (AM) was evaluated at 6 hours following blast injury by assessing the expression of catecholamine biosynthesizing enzymes, tyrosine hydroxylase (TH), dopamine‐β hydroxylase (DβH), along with Neuropeptide Y (NPY). TH and DβH expression increased by 20% and 25%, respectively, following OBI (P<0.05). NPY expression was also significantly elevated by 91% ( P <0.01) following OBI. NPY is synthesized and co‐realesed with catecholamines in the AM. Collectively, the increased TH, DβH and NPY expression in the rat AM suggests that OBI results in increased sympathoexcitation. Such effects may be one of the important factors contributing to autonomic dysfunction following OBI.