title: Role of nucleus of the solitary tract noradrenergic neurons in post-stress cardiovascular and hormonal control in male rats.
abstract: Chronic stress causes hypothalamo-pituitary-adrenal (HPA) axis hyperactivity and cardiovascular dyshomeostasis. Noradrenergic (NA) neurons in the nucleus of the solitary tract (NTS) are considered to play a role in these changes. In this study, we tested the hypothesis that NTS NA A2 neurons are required for cardiovascular and HPA axis responses to both acute and chronic stress. Adult male rats received bilateral microinjection into the NTS of 6-hydroxydopamine (6-OHDA) to lesion A2 neurons [cardiovascular study, n = 5; HPA study, n = 5] or vehicle [cardiovascular study, n = 6; HPA study, n = 4]. Rats were exposed to acute restraint stress followed by 14 d of chronic variable stress (CVS). On the last day of testing, rats were placed in a novel elevated plus maze (EPM) to test post-CVS stress responses. Lesions of NTS A2 neurons reduced the tachycardic response to acute restraint, confirming that A2 neurons promote sympathetic activation following acute stress. In addition, CVS increased the ratio of low-frequency to high-frequency power for heart rate variability, indicative of sympathovagal imbalance, and this effect was significantly attenuated by 6-OHDA lesion. Lesions of NTS A2 neurons reduced acute restraint-induced corticosterone secretion, but did not affect the corticosterone response to the EPM, indicating that A2 neurons promote acute HPA axis responses, but are not involved in CVS-mediated HPA axis sensitization. Collectively, these data indicate that A2 neurons promote both cardiovascular and HPA axis responses to acute stress. Moreover, A2 catecholaminergic neurons may contribute to the potentially deleterious enhancement of sympathetic drive following chronic stress.
authors.affiliation: Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati Metabolic Diseases Institute , Cincinnati, OH , USA and.
authors.forename: Jana
authors.initials: J
authors.lastname: Bundzikova-Osacka
authors.forename: Sriparna
authors.initials: S
authors.lastname: Ghosal
authors.forename: Benjamin A
authors.initials: BA
authors.lastname: Packard
authors.forename: Yvonne M
authors.initials: YM
authors.lastname: Ulrich-Lai
authors.forename: James P
authors.initials: JP
authors.lastname: Herman
mesh_terms: D059331:Adrenergic Neurons / Q000187:drug effects* / Q000502:physiology; D000818:Animals; D002319:Cardiovascular System; D003345:Corticosterone / Q000378:metabolism; D006339:Heart Rate / Q000187:drug effects* / Q000502:physiology; D007030:Hypothalamo-Hypophyseal System / Q000187:drug effects / Q000378:metabolism; D008297:Male; D016627:Oxidopamine / Q000494:pharmacology*; D010913:Pituitary-Adrenal System / Q000187:drug effects / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D017552:Solitary Nucleus / Q000166:cytology / Q000187:drug effects* / Q000502:physiology; D013312:Stress, Physiological / Q000187:drug effects* / Q000502:physiology; D013315:Stress, Psychological; D013565:Sympatholytics / Q000494:pharmacology*
chemical_list: D013565:Sympatholytics; D016627:Oxidopamine; D003345:Corticosterone
keywords: Acute stress; chronic variable stress; corticosterone; elevated plus maze; heart rate; heart rate variability