title: Effect of chronic forced running on gene expression of catecholamine biosynthetic enzymes in stellate ganglia of rats.
abstract: The sympathoneural system has a profound influence on the heart function. Sympathetic neurons are the major contributors to the huge rise of circulating noradrenaline (NA) level in response to stressful stimuli. Treadmill training in rats is forced exercise which has the propensity to induce both psychological and physical stress. The aim of this study is to examine how chronic forced running (CFR) affects the expression of catecholamine biosynthetic enzymes (tyrosine hydroxylase (TH), dopamine-beta-hydroxylase (DBH) and phenylethanolamine N-methyltransferase (PNMT)) and cAMP response element-binding (CREB) in stellate ganglia, as well as the concentrations of catecholamines, adrenocorticotropic hormone (ACTH) and corticosterone (CORT) in the plasma of rats. Also, we investigated how the additional acute immobilization stress changes the mentioned parameters. The rat training program consisted of 12 weeks running on a treadmill (20 m/min, 20 min/day). We found that CFR increases TH and DBH mRNA and protein levels in stellate ganglia, which is followed by increased NA concentration in the plasma. CFR reduces the level of PNMT mRNA, while the level of PNMT protein remains unchanged in stellate ganglia. The increased expression of TH and DBH genes positively correlates with the expression of CREB in stellate ganglia and with plasma ACTH level, while reduced level of PNMT mRNA in stellate ganglia correlates with reduced plasma CORT level. The additional acute immobilization stress increased gene expression of catecholamine biosynthetic enzymes in stellate ganglia, as well as catecholamines, ACTH and CORT levels in the plasma. The results presented here suggest that the continuous increase of the noradrenaline biosynthetic enzyme expression in stellate ganglia due to CFR may play a role in growing risk of cardiovascular diseases.
authors.affiliation: Institute of Nuclear Sciences Vinca, University of Belgrade, Belgrade, Serbia. gljubica@vinca.rs
authors.forename: L
authors.initials: L
authors.lastname: Gavrilovic
authors.forename: V
authors.initials: V
authors.lastname: Mandusic
authors.forename: V
authors.initials: V
authors.lastname: Stojiljkovic
authors.forename: J
authors.initials: J
authors.lastname: Kasapovic
authors.forename: S
authors.initials: S
authors.lastname: Stojiljkovic
authors.forename: S B
authors.initials: SB
authors.lastname: Pajovic
authors.forename: S
authors.initials: S
authors.lastname: Dronjak
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000097:blood; D000818:Animals; D002318:Cardiovascular Diseases / Q000097:blood / Q000201:enzymology* / Q000209:etiology; D002395:Catecholamines / Q000096:biosynthesis*; D003345:Corticosterone / Q000097:blood; D015971:Gene Expression Regulation, Enzymologic; D008297:Male; D010805:Physical Conditioning, Animal / Q000009:adverse effects*; D051381:Rats; D017208:Rats, Wistar; D013233:Stellate Ganglion / Q000378:metabolism* / Q000473:pathology
chemical_list: D002395:Catecholamines; D000324:Adrenocorticotropic Hormone; D003345:Corticosterone