Afferent signaling drives oxytocinergic preautonomic neurons and mediates training-induced plasticity

被引:31
|
作者
Cavalleri, Marina T. [1 ]
Burgi, Katia [1 ]
Cruz, Josiane C. [1 ]
Jordao, Maria T. [1 ]
Ceroni, Alexandre [1 ]
Michelini, Lisete C. [1 ]
机构
[1] Univ Sao Paulo, Dept Physiol & Biophys, Inst Biomed Sci, BR-05508000 Sao Paulo, Brazil
基金
巴西圣保罗研究基金会;
关键词
sinoaortic denervation; exercise training; hypothalamus; paraventricular nucleus; supraoptic nucleus; oxytocin; spontaneous hypertension; NUCLEUS-TRACTUS-SOLITARIUS; CARDIOVASCULAR CONTROL; HEART-RATE; EXERCISE; VASOPRESSIN; PRESSURE; EXPRESSION; RESPONSES; HYPERTENSION; ADJUSTMENTS;
D O I
10.1152/ajpregu.00104.2011
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Cavalleri MT, Burgi K, Cruz JC, Jordao MT, Ceroni A, Michelini LC. Afferent signaling drives oxytocinergic preautonomic neurons and mediates training-induced plasticity. Am J Physiol Regul Integr Comp Physiol 301: R958-R966, 2011. First published July 27, 2011; doi:10.1152/ajpregu.00104.2011.-We showed previously that oxytocinergic (OTergic) projections from the hypothalamic paraventricular nucleus (PVN) to the dorsal brain stem mediate traininginduced 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.
引用
收藏
页码:R958 / R966
页数:9
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