Role of nucleus of the solitary tract noradrenergic neurons in post-stress cardiovascular and hormonal control in male rats.
Role of nucleus of the solitary tract noradrenergic neurons in post-stress cardiovascular and hormonal control in male rats.
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DOI：
10.3109/10253890.2015.1013531
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发表时间：
2015
期刊：
影响因子：
--
通讯作者：
Herman JP
中科院分区：
文献类型：
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作者：
Bundzikova-Osacka J;Ghosal S;Packard BA;Ulrich-Lai YM;Herman JP
慢性应激可引起下丘脑-垂体-肾上腺（HPA）轴功能亢进和心血管稳态失调。孤束核（NTS）中的去甲肾上腺素能神经元被认为在这些变化中发挥作用。在这里，我们测试的假设，NTS去甲肾上腺素能A2神经元所需的心血管和HPA轴的反应，急性和慢性应激。成年雄性大鼠接受双侧NTS微量注射6-羟基多巴胺（6-OHDA）以损伤A2神经元[心血管研究，n= 5; HPA研究，n= 5]或溶剂[心血管研究，n= 6; HPA研究，n= 4]。将大鼠暴露于急性束缚应激，然后进行14天的慢性可变应激（CVS）。在测试的最后一天，将大鼠置于新型高架十字迷宫（elevated plus maze）中以测试CVS后应激反应。NTS A2神经元的病变减少了对急性束缚的心动过速反应，证实了A2神经元在急性应激后促进交感神经激活。此外，CVS增加了心率变异性的低频与高频功率的比值，表明交感迷走神经失衡，这种影响被6-OHDA损伤显著减弱。NTS A2神经元的损伤减少了急性束缚诱导的皮质酮分泌，但不影响皮质酮的反应，表明A2神经元促进急性HPA轴反应，但不参与CVS介导的HPA轴敏化。总的来说，这些数据表明，A2神经元促进心血管和HPA轴对急性应激的反应。此外，A2儿茶酚胺能神经元可能有助于慢性应激后交感神经驱动的潜在有害增强。
Chronic stress causes hypothalamo-pituitary-adrenal (HPA) axis hyperactivity and cardiovascular dyshomeostasis. Noradrenergic neurons in the nucleus of the solitary tract (NTS) are considered to play a role in these changes. Here, we tested the hypothesis that NTS noradrenergic 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 days 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.