To study the positive feed-back mechanism by which oestrogen induces corpus luteum formation, electrolytic lesions were placed in different parts of the anterior hypothalamus of prepubertal female rats which were then injected with oestradiol benzoate. Ovarian luteinization did not occur when the main parts of the suprachiasmatic nuclei or of the medial preoptic area had been destroyed.Oestradiol benzoate was implanted stereotaxically into the brain and the anterior pituitary of immature female rats. Whereas 1/25 of the subcutaneously effective dose had to be implanted into the anterior hypothalamus, 1/100 of the peripherally effective dose introduced into the adenohypophysis was sufficient to induce corpus luteum formation in most of the treated animals.The results suggest that, although the anterior hypothalamus is necessary for this positive feed-back mechanism, the anterior pituitary may be the main site of action of oestrogen.Oestrogen may increase the hypophysial sensitivity to the hypothalamic gonadotrophin-releasing factor. Thus an enhanced gonadotrophin secretion may result, sufficient for the induction of ovulation. The possibility is discussed that this positive feed-back mechanism is also essential for the induction of ovulation in women.
Bilateral lesions placed in the medial preoptic area (MPOA) markedly diminished the luteinizing hormone-(LH-) and follicle-stimulating hormone- (FSH-) inhibiting effects of s.c. injected or intrahypothalamically implanted estradiol benzoate (EB) in ovariectomized immature rats. Desensitization to the negative estrogen feedback was also recorded in immature rats implanted into the MPOA with a mixture of 1 part EB and 240 or 360 parts cholesterol. Estrogen implants located in the hypothalamic ventromedial-arcuate region were ineffective in this regard. Whereas precocious puberty resulted from the implantation of EB into the MPOA, a delay of puberty onset was induced by medial preoptic implants of the antiestrogen clomiphene citrate which also enhanced the LH-suppressing effect of s.c. administered EB in prepubertal females. It is proposed that an increase of the estrogen concentration in the MPOA inactivates medial preoptic neurons that exert a restraining influence on tonic LH (and FSH) secretion by sensitizing the mediobasal hypothalamus to the negative feedback action of estrogen. This mechanism may be involved in the control of the onset of puberty in female rats.
The puberty-controlling function of the mediocortical amygdala in immature female rats was investigated by lesioning this region at different ages and by studying the effects on the onset of spontaneous and experimentally-induced precocious puberty. At 21 days of age, bilateral lesions in the anterior mediocortical amygdala (AMCA) caused precocious puberty and enhanced the puberty-accelerating effect of bilateral lesions produced simultaneously in the medial preoptic area (MPA). Similar lesions, ineffective on day 26, delayed the onset of puberty when produced on day 32 in otherwise untreated rats. Lesions in the posterior mediocortical amygdala (PMCA) at 26 or 32 days of age postponed puberty in untreated rats and inhibited the advancement of their 1st pubertal ovulation that resulted from damage to the ventromedial-arcuate region (VAH) or daily administration of 0.05 µg estradiol benzoate (EB) per 100 g b.w. The results confirm earlier findings of different gonadotropin-controlling activities of the AMCA and PMCA in immature female rats and suggest maturational changes in the function of both areas. The gonadotropin-inhibiting action exerted by the AMCA at 3 weeks of age is lost when puberty approaches; a gonadotropin-stimulating activity seems to develop in both the AMCA and PMCA.
Implantation of testosterone propionate (tp) in the pre-optic-anterior hypothalamic region produced predominantly male, i.e. homosexual behaviour in female spayed rats. On the other hand, tp implants in the central hypothalamus induced mainly female behaviour, as did subcutaneous tp injections in these animals (D\l=o"\rner, D\l=o"\cke& Moustafa, 1968). Therefore, it was assumed that two different hypothalamic mating centres are responsible for the male and female mating activity. In the following study this hypothesis was reinvestigated by means of intra-hypothalamic implantations of oestradiol benzoate (ob) in rats.Precise quantities of crystalline ob were implanted stereotaxically into the anterior or central hypothalamus of post-puberally spayed female rats of the Sprague-Dawley strain. The stereotaxic implantations were performed according to a method described recently (D\l=o"\cke, D\l=o"\rner& Voigt, 1968). ob was dissolved in alcohol, the solution was aspirated into calibrated glass capillary tubes, and the hormone was implanted after evaporation of the alcohol and recrystallization. The implants were introduced bilaterally anterior or posterior to the bregma according to the stereotaxic atlas of Szent\l=a'\gothai,Flerk\l=o'\, Mess & Hal\l=a'\sz (1968) (A 0\m=.\5for implantations in the anterior and P 2\m=.\5in the central (middle) hypothalamus). After autopsy each hypothalamus was frozen, serially sectioned at 15 \g=m\ and stained with haematoxylin and eosin to verify the exact localization of the implants.Tests for sexual behaviour were performed on Days 3, 5 and 7 following the implantation. In the mating tests each rat was exposed for 5 min to (1) a vigorous male, and (2) an oestrous female (Dörner, 1967). Animals with intra¬ hypothalamic cholesterol implants or subcutaneous ob implants served as
Bilateral lesions produced with a platinum electrodewere placed in the anterior or central parts of the mediocortical amygdaloid nuclei, or in the anterior and basal region of the ventral hippocampus of 22-day-old female rats, and the effects on vaginal opening (VO), first puberal ovulation and subsequent vaginal cyclicity were recorded. Lesioning of the anterior part of the amygdaloid mediocortical nuclear complex resulted in precocious puberty, whereas lesions located in the central parts of these nuclei did not influence the onset of puberty. On the other hand, a significant delay of VO and the first ovulation was observed after bilateral hippocampal damage. The results suggest an inhibitory action of the anterior mediobasal amygdala on the prepuberal gonadotropin secretion and indicate a reciprocal relationship between the anterior amygdala and the ventral hippocampus in the control of female puberty.
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