González-Quijano M I, Ariznavarreta C, Martín A I, Treguerres J A, López-Calderón A
Departamento de Enfermeria, Escuela Universitaria de Enfermeria, Madrid, Spain.
Neuroendocrinology. 1991 Nov;54(5):447-53. doi: 10.1159/000125933.
There is considerable evidence suggesting that endogenous opioids may play an important role in acute stress-induced decreases in luteinizing hormone (LH) release. Studies were undertaken to analyze the role of endogenous opioids in chronic stress-induced decrease in circulating LH and follicle-stimulating hormone (FSH). Chronic restraint (6 h daily over 4 days) evoked a decrease in circulating LH and FSH. Naltrexone treatment, (2 mg/kg three times daily) during the 4 days of restraint, caused an increase in plasma concentrations of LH and FSH, and antagonized the LH suppressory effect of morphine (10 mg/kg) administration. Despite this, naltrexone treatment was ineffective in preventing the inhibitory effect of chronic restraint stress on circulating LH and FSH. Chronic restraint also induced a decrease in hypothalamic LH-releasing hormone (LHRH) content in saline-treated rats. On the contrary, in naltrexone-treated rats, chronic restraint evoked an increase in hypothalamic LHRH content. Thus endogenous opioids and chronic stress seem to act by different mechanisms on the hypothalamic LHRH neuron. In unstressed orchidectomized rats, naltrexone administration did not modify circulating LH, but increased plasma concentrations of LH in acutely restrained rats. These data suggest that endogenous opioids may mediate gonadotropin secretion during acute stress, but not during chronic stress.
有大量证据表明，内源性阿片类物质可能在急性应激诱导的促黄体生成素（LH）释放减少中起重要作用。本研究旨在分析内源性阿片类物质在慢性应激诱导的循环中LH和促卵泡生成素（FSH）减少中的作用。慢性束缚（连续4天每天6小时）导致循环中LH和FSH减少。在束缚的4天期间，纳曲酮治疗（每天3次，每次2mg/kg）使LH和FSH的血浆浓度升高，并拮抗了吗啡（10mg/kg）给药对LH的抑制作用。尽管如此，纳曲酮治疗在预防慢性束缚应激对循环中LH和FSH的抑制作用方面无效。慢性束缚还导致生理盐水处理的大鼠下丘脑促性腺激素释放激素（LHRH）含量降低。相反，在纳曲酮处理的大鼠中，慢性束缚使下丘脑LHRH含量增加。因此，内源性阿片类物质和慢性应激似乎通过不同机制作用于下丘脑LHRH神经元。在未受应激的去势大鼠中，纳曲酮给药并未改变循环中的LH，但在急性束缚的大鼠中增加了LH的血浆浓度。这些数据表明，内源性阿片类物质可能在急性应激期间介导促性腺激素分泌，但在慢性应激期间则不然。
