Lacau-Mengido I M, González Iglesias A, Díaz-Torga G, Thyssen-Cano S, Libertun C, Becú-Villalobos D
Laboratorio de Neuroendocrinología, Instituto de Biología y Medicina Experimental, CONICET, Buenos Aires, Argentina.
Proc Soc Exp Biol Med. 1998 Apr;217(4):445-9. doi: 10.3181/00379727-217-44255.
Marked sexual and ontogenic differences have been described in gonadotropin regulation in the rat. These could arise from events occurring both at the hypothalamic or hypophyseal levels. The present experiments were designed to evaluate the capacity of the hypothalamus in releasing GnRH in vitro, basally and in response to depolarization with KCl, during ontogeny in the rat. To that end we chose two well-defined developmental ages that differ markedly in sexual and ontogenic characteristics of gonadotropin regulation, 15 and 30 days. We compared GnRH release from hypothalami of females, neonatal androgenized females and males. Mediobasal hypothalami were perifused in vitro, and GnRH measured in the effluent. Basal secretion of the decapeptide increased with age in the three groups with no sexual differences encountered. When studying GnRH release induced by membrane depolarization, no differences within sex or age were encountered. On the other hand FSH serum levels decreased with age in females and increased in males, and in neonatal androgenized females followed a similar pattern to that of females. LH levels were higher in infantile females than in age-matched males or androgenized females. Such patterns of gonadotropin release were therefore not correlated to either basal or K+-induced GnRH release from the hypothalamus. We conclude that sexual and ontogenic differences in gonadotropin secretion in the developing rat are not dependent on the intrinsic capability of the hypothalamus to release GnRH in response to membrane depolarization. The hormonal differences observed during development and between sexes are probably related to differences in the sensitivity of the GnRH neuron to specific secretagogue and neurotransmitter regulation, and/or to differences in hypophyseal GnRH receptors and gonadotrope sensitivity.
在大鼠促性腺激素调节方面，已描述了明显的性别和个体发育差异。这些差异可能源于下丘脑或垂体水平发生的事件。本实验旨在评估大鼠个体发育过程中下丘脑在体外基础状态下以及对氯化钾去极化反应时释放促性腺激素释放激素（GnRH）的能力。为此，我们选择了两个明确界定的发育年龄，它们在促性腺激素调节的性别和个体发育特征上有显著差异，即15天和30天。我们比较了雌性、新生期雄激素化雌性和雄性大鼠下丘脑GnRH的释放情况。将中基底部下丘脑进行体外灌流，并测量流出液中的GnRH。三组中十肽的基础分泌均随年龄增加，未发现性别差异。在研究膜去极化诱导的GnRH释放时，未发现性别或年龄组内有差异。另一方面，雌性血清促卵泡生成素（FSH）水平随年龄下降，雄性则升高，新生期雄激素化雌性的变化模式与雌性相似。婴儿期雌性的促黄体生成素（LH）水平高于年龄匹配的雄性或雄激素化雌性。因此，这种促性腺激素释放模式与下丘脑基础或钾离子诱导的GnRH释放均无相关性。我们得出结论，发育中大鼠促性腺激素分泌的性别和个体发育差异并不取决于下丘脑对膜去极化反应释放GnRH的内在能力。发育过程中以及两性之间观察到的激素差异可能与GnRH神经元对特定促分泌素和神经递质调节的敏感性差异，和/或与垂体GnRH受体及促性腺激素细胞敏感性差异有关。
