Karteszi M, Palkovits M, Kiss J Z, Kanyicska B, Fekete M I, Stark E
Neuroendocrinology. 1981 Jan;32(1):7-13. doi: 10.1159/000123121.
The central serotonergic system was manipulated using a serotonin receptor antagonist (cyproheptadine), electrolytic lesioning of the raphe nuclei and neurochemical destruction of the serotonergic terminals in the hypothalamus. The effects of these interventions on ether-induced ACTH secretion were studied in adrenalectomized rats. Serotonin, norepinephrine and dopamine concentrations were measured in the medial basal hypothalamus (MBH) or in individual nuclei of the hypothalamus and of certain midbrain regions. Cyproheptadine pretreatment inhibited ether-induced ACTH hypersecretion in adrenalectomized animals. Neither the electrolytic lesions of the midbrain raphe nuclei, nor the neurotoxic destruction of the hypothalamic serotonergic terminals (by intraventricular administration of 5,6-dihydroxytryptamine) caused any alteration of stimulated ACTH secretion after ether inhalation and/or long-term corticoid deficiency. These results suggest a lack of correlation between the activity of the central serotonergic system and the ACTH releasing effect of ether-stress in adrenalectomized rats.
使用5-羟色胺受体拮抗剂(赛庚啶)、中缝核的电解损伤以及下丘脑5-羟色胺能终末的神经化学破坏来调控中枢5-羟色胺能系统。在肾上腺切除的大鼠中研究了这些干预措施对乙醚诱导的促肾上腺皮质激素(ACTH)分泌的影响。测定了内侧基底下丘脑(MBH)或下丘脑及某些中脑区域的单个核团中的5-羟色胺、去甲肾上腺素和多巴胺浓度。赛庚啶预处理可抑制肾上腺切除动物中乙醚诱导的ACTH分泌过多。中脑缝际核的电解损伤以及下丘脑5-羟色胺能终末的神经毒性破坏(通过脑室内注射5,6-二羟基色胺)均未引起乙醚吸入和/或长期皮质激素缺乏后刺激的ACTH分泌发生任何改变。这些结果表明,在肾上腺切除的大鼠中,中枢5-羟色胺能系统的活性与乙醚应激的ACTH释放效应之间缺乏相关性。