title: Afferent signaling drives oxytocinergic preautonomic neurons and mediates training-induced plasticity.
abstract: We showed previously that oxytocinergic (OTergic) projections from the hypothalamic paraventricular nucleus (PVN) to the dorsal brain stem mediate training-induced heart rate (HR) adjustments and that beneficial effects of training are blocked by sinoaortic denervation (SAD; Exp Physiol 94: 630-640; 1103-1113, 2009). We sought now to determine the combined effect of training and SAD on PVN OTergic neurons in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. Rats underwent SAD or sham surgery and were trained (55% of maximal capacity) or kept sedentary for 3 mo. After hemodynamic measurements were taken at rest, rats were deeply anesthetized. Fresh brains were frozen and sliced to isolate the PVN; samples were processed for OT expression (real-time PCR) and fixed brains were processed for OT immunofluorescence. In sham rats, training improved treadmill performance and increased the gain of baroreflex control of HR. Training reduced resting HR (-8%) in both groups, with a fall in blood pressure (-10%) only in SHR rats. These changes were accompanied by marked increases in PVN OT mRNA expression (3.9- and 2.2-fold in WKY and SHR rats, respectively) and peptide density in PVN OTergic neurons (2.6-fold in both groups), with significant correlations between OT content and training-induced resting bradycardia. SAD abolished PVN OT mRNA expression and markedly reduced PVN OT density in WKY and SHR. Training had no effect on HR, PVN OT mRNA, or OT content following SAD. The chronic absence of inputs from baroreceptors and chemoreceptors uncovers the pivotal role of afferent signaling in driving both the plasticity and activity of PVN OTergic neurons, as well as the beneficial effects of training on cardiovascular control.
authors.affiliation: Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.
authors.forename: Marina T
authors.initials: MT
authors.lastname: Cavalleri
authors.forename: Katia
authors.initials: K
authors.lastname: Burgi
authors.forename: Josiane C
authors.initials: JC
authors.lastname: Cruz
authors.forename: Maria T
authors.initials: MT
authors.lastname: Jordão
authors.forename: Alexandre
authors.initials: A
authors.lastname: Ceroni
authors.forename: Lisete C
authors.initials: LC
authors.lastname: Michelini
mesh_terms: D000818:Animals; D017776:Autonomic Pathways / Q000378:metabolism*; D001794:Blood Pressure / Q000502:physiology; D003714:Denervation; D004195:Disease Models, Animal; D006339:Heart Rate / Q000502:physiology; D006973:Hypertension / Q000503:physiopathology; D008297:Male; D023421:Models, Animal; D009473:Neuronal Plasticity / Q000502:physiology*; D009475:Neurons, Afferent / Q000502:physiology*; D010121:Oxytocin / Q000378:metabolism*; D010286:Paraventricular Hypothalamic Nucleus / Q000502:physiology; D010805:Physical Conditioning, Animal / Q000502:physiology*; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D015398:Signal Transduction / Q000502:physiology*; D012849:Sinoatrial Node / Q000502:physiology / Q000601:surgery; D013495:Supraoptic Nucleus / Q000502:physiology
chemical_list: D010121:Oxytocin