Sympathetic nervous system contributes to enhanced corticosterone levels following chronic stress.
Sympathetic nervous system contributes to enhanced corticosterone levels following chronic stress.
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DOI：
10.1016/j.psyneuen.2016.02.027
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发表时间：
2016-06
影响因子：
3.7
通讯作者：
Johnson JD
中科院分区：
文献类型：
--
作者：
Lowrance SA;Ionadi A;McKay E;Douglas X;Johnson JD
暴露于慢性应激通常会在昼夜节律最低点时升高基础循环糖皮质激素，并在暴露于后续应激源后导致糖皮质激素分泌过高。虽然糖皮质激素的产生主要由下丘脑-垂体-肾上腺（HPA）轴介导，但有证据表明交感神经系统可以通过直接作用于肾上腺来影响糖皮质激素的昼夜产生。本实验旨在研究慢性应激后HPA和交感神经系统在促进皮质酮生成中的作用。将大鼠置于为期4天的应激模式或对照条件下，然后在第5天置于急性约束应激下，观察皮质酮和促肾上腺皮质激素的反应。在昼夜节律的最低点，反复的应激源暴露导致皮质酮的少量增加，但ACTH没有增加，并且在限制性应激后的5、10和20分钟内也导致皮质酮的过量产生。虽然抑制5分钟后循环ACTH水平升高，但直到20分钟后，慢性应激动物的水平才比对照组高。在慢性应激动物中，在限制性应激前给予应激素（一种CRH拮抗剂）可显著降低ACTH反应，但不能阻止皮质酮的致敏性反应。相比之下，氯异丹明（一种神经节阻滞剂）使慢性应激动物的基础皮质酮水平恢复到正常水平，并在抑制（长达10分钟）后减少早期皮质酮的产生，但在慢性应激动物20分钟时没有阻断过度的皮质酮反应。这些数据表明，交感神经系统张力的增加有助于慢性应激后糖皮质激素的基础和快速产生，但HPA反应可能介导皮质酮对持续时间较长的应激源的峰值反应。
Exposure to chronic stress often elevates basal circulating glucocorticoids during the circadian nadir and leads to exaggerated glucocorticoid production following exposure to subsequent stressors. While glucocorticoid production is primarily mediated by the hypothalamic–pituitary–adrenal (HPA) axis, there is evidence that the sympathetic nervous system can affect diurnal glucocorticoid production by direct actions at the adrenal gland. Experiments here were designed to examine the role of the HPA and sympathetic nervous system in enhancing corticosterone production following chronic stress. Rats were exposed to a four-day stress paradigm or control conditions then exposed to acute restraint stress on the fifth day to examine corticosterone and ACTH responses. Repeated stressor exposure resulted in a small increase in corticosterone, but not ACTH, during the circadian nadir, and also resulted in exaggerated corticosterone production 5, 10, and 20 min following restraint stress. While circulating ACTH levels increased after 5 min of restraint, levels were not greater in chronic stress animals compared to controls until following 20 min. Administration of astressin (a CRH antagonist) prior to restraint stress significantly reduced ACTH responses but did not prevent the sensitized corticosterone response in chronic stress animals. In contrast, administration of chlorisondamine (a ganglionic blocker) returned basal corticosterone levels in chronic stress animals to normal levels and reduced early corticosterone production following restraint (up to 10 min) but did not block the exaggerated corticosterone response in chronic stress animals at 20 min. These data indicate that increased sympathetic nervous system tone contributes to elevated basal and rapid glucocorticoid production following chronic stress, but HPA responses likely mediate peak corticosterone responses to stressors of longer duration.
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