Serotonergic involvement in stress-induced ACTH release
Serotonergic involvement in stress-induced ACTH release
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DOI：
10.1016/s0006-8993(98)00901-9
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发表时间：
1998-11-16
期刊：
影响因子：
2.9
通讯作者：
Warberg, J
中科院分区：
文献类型：
--
作者：
Jorgensen, H;Knigge, U;Warberg, J
我们研究了成年雄性大鼠中血清素 (5-MT) 和 5-HT 受体在介导应激诱导的 ACTH 分泌中的作用，这些大鼠在束缚应激、乙醚应激、冷游泳应激或内毒素之前先用 5-HT 拮抗剂进行预处理。所有压力源都会显着增加血浆 ACTH。用脑室内、室旁核或中缝核注射 5,7-二羟色胺损伤 5-HT 神经元，抑制束缚应激诱导的 ACTH 反应达 50%。约束增加了中缝核中 5-HT 及其代谢物 5-羟基吲哚乙酸的含量，而其他应激源则没有这种作用。用 5-MT1A 受体拮抗剂 WAY 100635 预处理可抑制束缚应激和内毒素诱导的 ACTH 分泌 50%。 5-HT1+2拮抗剂美西麦角或5-HT2拮抗剂酮色林抑制束缚或乙醚应激诱导的ACTH反应，并消除内毒素诱导的ACTH反应。 5-MT3 受体拮抗剂 LY 53857 仅阻断内毒素诱导的 ACTH 反应。用 5-MT3 受体拮抗剂昂丹司酮进行预处理对应激刺激的 ACTH 分泌没有影响。 5-MT3+4 受体拮抗剂托烷司酮抑制束缚应激和乙醚应激诱导的反应。 ACTH 对游泳压力的反应不受任何所用拮抗剂的影响。结论是5-MT1A、5-MT2C和5-MT3受体参与应激诱导的ACTH分泌，但5-MT3受体不参与。 5-MT4 受体可能参与其中。此外，中缝核中的血清素能神经元在束缚应激期间被激活，并且这些神经元和下丘脑 PVN 中的神经元对于调节束缚应激诱导的 ACTH 反应非常重要。 (C) 1998 Elsevier Science B.V. 保留所有权利。
We investigated the involvement of serotonin (5-MT) and 5-HT receptors in mediation of stress-induced ACTH secretion in adult male rats, which were pretreated by 5-HT antagonists before restraint-, ether-, cold swim-stress or endotoxin. All stressors potently increased plasma ACTH. Lesion of 5-HT neurons with 5,7-dihydroxytryptamine injected intracerebroventricularly, into the paraventricular nucleus or into the raphe nuclei, inhibited the restraint stress-induced ACTH response by 50%. Restraint increased the content of 5-HT and its metabolite 5-hydroxyindole acetic acid, in the raphe nuclei, whereas the other stressors had no such effect. Pretreatment with the 5-MT1A receptor antagonist WAY 100635 inhibited the restraint stress- and endotoxin-induced ACTH secretion by 50%. The 5-HT1+2 antagonist methysergide or the 5-HT2 antagonist ketanserin inhibited the restraint- or ether stress-induced ACTH response, and eliminated the endotoxin-induced ACTH response. The 5-MT3 receptor antagonist LY 53857 blocked only the endotoxin-induced ACTH response. Pretreatment with the 5-MT3 receptor antagonist ondansetrone had no effect on stress-stimulated ACTH secretion. The 5-MT3+4 receptor antagonist tropisetrone inhibited the restraint- and ether stress-induced response. The ACTH response to swim stress was not affected by any of the antagonists used. It is concluded that the 5-MT1A, the 5-MT2C and the 5-MT3 receptor, but not the 5-MT3 receptor are involved in the stress-induced ACTH secretion. An involvement of the 5-MT4 receptor is possible. Furthermore, that serotonergic neurons in the raphe nuclei are activated during restraint stress, and that these neurons and neurons in PVN of the hypothalamus, are important for the mediation of the restraint stress-induced ACTH response. (C) 1998 Elsevier Science B.V. All rights reserved.