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  • Title: Studies on the puberty-controlling function of the mediocortical amygdala in the immature female rat.
    Author: Döcke F, Lemke M, Okrasa R.
    Journal: Neuroendocrinology; 1976; 20(2):166-75. PubMed ID: 986578.
    Abstract:
    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 mug 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. Vaginal openings and the 1st pubertal ovulations usually occurred between 38-42 days of age in female Wistar rats. Autopsies were done on the 16th day after vaginal openings were detected, or on the day of vaginal estrus after the 1st pubertal ovulation. For daily long-term treatment with estradiol benzoate sc injections of .05 mcg were given, with higher doses as age advanced. Bilateral lesions were produced by passing an anodal DC of 1 mA through a unipolar platinum electrode. 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. Similar lesions were ineffective on Day 26, but when produced on Day 32 they delayed the onset of puberty. Lesions of the posterior mediocortical amygdala (PMCA) at 26 or 32 days of age delayed puberty and inhibited the advancement of the 1st pubertal ovulation that had resulted from damage to the ventromedial-arcuate region, or by the daily administration of .05 mc of estradiol/benzoate/100 gm body weight. Results showed different gonadotropin-controlling activities of the AMCA and PMCA in prepubertal female rats. The gonadotropin-inhibitory action exerted by AMCA at 3 weeks of age was lost when puberty approached. Maturational changes in the function of both areas seemed to develop.
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