Herdon H J, Everard D M, Wilson C A
J Endocrinol. 1984 Feb;100(2):235-44. doi: 10.1677/joe.0.1000235.
The effects of castration with or without testosterone replacement in the adult male rat were studied to investigate possible hypothalamic mechanisms by which changes in gonadotrophin secretion occur at different times after castration, with particular reference to the continuing LH rise and its lack of suppression by testosterone in the long-term castrated rat. Castrated rats received either subcutaneous silicone elastomer implants containing testosterone or empty implants at the time of castration, and a sham-operated group served as controls. At 1, 10 and 40 days after castration, there were six-, 15- and 25-fold rises respectively in LH and 1.5-, two- and fivefold rises in FSH. However, there were no significant changes in hypothalamic noradrenaline concentration and turnover or in alpha-adrenoceptor density and affinity at any time after castration. Testosterone implants were effective in suppressing gonadotrophin release at 1 and 10 days, but not at 40 days after castration, and did not significantly affect hypothalamic noradrenaline turnover or alpha-adrenoceptors at any time. Neither acute inhibition of the noradrenergic system, using either the alpha-adrenoceptor blockers phenoxybenzamine and phentolamine or the synthesis inhibitor alpha-methyl-p-tyrosine, nor chronic depletion of hypothalamic noradrenaline by 6-hydroxydopamine had any significant effect on the normal rise in LH levels seen on days 10 and 40 after castration, and did not alter the ability of testosterone to suppress LH levels. This indicates that, in the long-term castrated rat, the noradrenergic system may not be involved in the control of gonadotrophin release. However, at 16 h after castration, alpha-adrenoceptor blockers and alpha-methyl-p-tyrosine did reduce LH levels, indicating that the noradrenergic system is likely to be involved in the short-term response to castration.
研究了成年雄性大鼠去势后补充或不补充睾酮的影响，以探讨促性腺激素分泌在去势后不同时间发生变化的可能下丘脑机制，尤其关注长期去势大鼠中促黄体生成素（LH）持续升高以及睾酮对其缺乏抑制作用的情况。去势大鼠在去势时接受皮下植入含睾酮的硅橡胶弹性体植入物或空植入物，假手术组作为对照。去势后1天、10天和40天，LH分别升高6倍、15倍和25倍，促卵泡生成素（FSH）分别升高1.5倍、2倍和5倍。然而，去势后任何时间下丘脑去甲肾上腺素浓度、周转率或α-肾上腺素能受体密度及亲和力均无显著变化。睾酮植入物在去势后1天和10天有效抑制促性腺激素释放，但在40天时无效，且在任何时间均未显著影响下丘脑去甲肾上腺素周转率或α-肾上腺素能受体。使用α-肾上腺素能受体阻滞剂酚苄明和酚妥拉明或合成抑制剂α-甲基对酪氨酸对去甲肾上腺素能系统进行急性抑制，以及用6-羟基多巴胺对下丘脑去甲肾上腺素进行慢性耗竭，均对去势后10天和40天LH水平的正常升高无显著影响，也未改变睾酮抑制LH水平的能力。这表明，在长期去势大鼠中，去甲肾上腺素能系统可能不参与促性腺激素释放的调控。然而，在去势后16小时，α-肾上腺素能受体阻滞剂和α-甲基对酪氨酸确实降低了LH水平，表明去甲肾上腺素能系统可能参与了对去势的短期反应。
