Induction of adrenal tyrosine hydroxylase mRNA by single immobilization stress occurs even after splanchnic transection and in the presence of cholinergic antagonists

• Published in: Journal of neurochemistry Vol. 66; no. 1; p. 138
• Main Authors: Kvetnanský, R, Nankova, B, Hiremagalur, B, Viskupic, E, Vietor, I, Rusnak, M, McMahon, A, Kopin, I J, Sabban, E L
• Format: Journal Article
• Language: English
• Published: England 01.01.1996
• Subjects: Adrenal Medulla - drug effects; Adrenal Medulla - enzymology; Adrenal Medulla - innervation; Animals; Atropine - pharmacology; Catecholamines - blood; Catecholamines - metabolism; Chlorisondamine - pharmacology; Cholinergic Antagonists - pharmacology; Cold Temperature; Enzyme Induction - drug effects; Immobilization; Male; Muscarinic Antagonists - pharmacology; Neuropeptide Y - biosynthesis; Neuropeptide Y - genetics; Nicotinic Antagonists - pharmacology; Rats; Rats, Sprague-Dawley; RNA, Messenger - biosynthesis; RNA, Messenger - genetics; Specific Pathogen-Free Organisms; Splanchnic Nerves - physiology; Stress, Physiological - physiopathology; Sympathectomy; Tyrosine 3-Monooxygenase - biosynthesis; Tyrosine 3-Monooxygenase - genetics
• ISSN: 0022-3042
• DOI: 10.1046/j.1471-4159.1996.66010138.x

Immobilization (IMO) stress elevates plasma catecholamines and increases tyrosine hydroxylase (TH) gene expression in rat adrenals. This study examined the mechanism(s) of IMO-induced changes in adrenal TH mRNA levels. Innervation of the adrenal medulla is predominantly cholinergic and splanchnicotomy as well as nicotinic receptor antagonists prevent the cold-induced rise in TH mRNA levels. In this study, the IMO-induced rise in plasma catecholamines, but not TH mRNA levels, was reduced by the antagonist chlorisondamine. Muscarinic antagonist atropine also did not prevent the IMO stress-elicited rise in TH mRNA. Furthermore, denervation of the adrenals by unilateral splanchnicotomy did not block the IMO-induced rise in TH mRNA but completely prevented the induction of neuropeptide Y mRNA. These results suggest that (1) the large increase in adrenal TH gene expression elicited by a single IMO stress is not regulated via cholinergic receptors or splanchnic innervation, and (2) there is a dissociation between regulatory mechanisms of catecholamine secretion and elevation of TH gene expression in the adrenal medulla of rats during IMO stress.