Sotowska-Brochocka J
Department of Animal Physiology, University of Warsaw, Poland.
Gen Comp Endocrinol. 1988 Apr;70(1):83-90. doi: 10.1016/0016-6480(88)90096-2.
In our previous experiments it was found that lesions placed in the infundibular hypothalamus induced an advanced ovulation in hibernating frogs, Rana temporaria. It was suggested that this premature ovulation was the effect of gonadotropin-releasing hormone (GnRH) due to the injury of some hypothalamic area inhibiting its release or its action on the pituitary gonadotrophs. To investigate this hypothesis, the following experiments were undertaken: (1) an attempt to induce ovulation with exogenous GnRH in hibernating frogs; (2) an attempt to inhibit ovulation with anti-GnRH serum in preovulatory hibernating animals nonlesioned and with lesions of the infundibular hypothalamus; and (3) administration of bromocriptine in hibernating animals to assess whether this substance, as an agonist of dopamine, possesses an inhibitory action on the ovulation. The following results were obtained: (1) lesions of the infundibular hypothalamus in hibernating preovulatory females caused an advanced ovulation during hibernation; (2) the exogenous GnRH administered to preovulatory females induced ovulation during hibernation; (3) the anti-GnRH serum injected into hibernating preovulatory lesioned females inhibited preterm ovulation during, but not after, hibernation; (4) the immunoneutralization of endogenous GnRH in nonlesioned females resulted in an inhibition of the posthibernatory ovulation; (5) bromocriptine inhibited posthibernatory ovulation in nonlesioned hibernating animals. Thus, the results of these experiments support the suggestion that induction of accelerated ovulation in lesioned hibernating animals involved the releasing action of GnRH. This action of GnRH seemed to be facilitated by the ablation of inhibitory dopaminergic function of hypothalamus in lesioned animals.
在我们之前的实验中发现,将损伤置于冬眠青蛙(林蛙)的漏斗下丘脑会诱导其提前排卵。有人提出,这种过早排卵是促性腺激素释放激素(GnRH)的作用,这是由于下丘脑某些区域受损,抑制了其释放或其对垂体促性腺细胞的作用。为了研究这一假设,我们进行了以下实验:(1)尝试用外源性GnRH诱导冬眠青蛙排卵;(2)尝试用抗GnRH血清抑制未受损和漏斗下丘脑受损的排卵前冬眠动物的排卵;(3)给冬眠动物注射溴隐亭,以评估这种作为多巴胺激动剂的物质是否对排卵具有抑制作用。获得了以下结果:(1)冬眠的排卵前雌性动物的漏斗下丘脑损伤导致冬眠期间提前排卵;(2)给排卵前雌性动物注射外源性GnRH可诱导冬眠期间排卵;(3)给冬眠的排卵前受损雌性动物注射抗GnRH血清可抑制冬眠期间的早产排卵,但不能抑制冬眠后的早产排卵;(4)对未受损雌性动物内源性GnRH进行免疫中和会导致冬眠后排卵受到抑制;(5)溴隐亭抑制未受损冬眠动物的冬眠后排卵。因此,这些实验结果支持了这样的观点,即受损冬眠动物中加速排卵的诱导涉及GnRH的释放作用。GnRH的这种作用似乎因受损动物下丘脑抑制性多巴胺能功能的消除而得到促进。