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  • Title: Changes in the concentration of LH, FSH and estrogen in the immature female rat during precocious sexual maturation induced by electrochemical stimulation of the brain.
    Author: YoungLai EV, Holmes MJ, Ruf KB.
    Journal: Horm Res; 1976; 7(1):34-42. PubMed ID: 1002115.
    Abstract:
    Electrochemical stimulation of the hypothalamus of 23-day-old female rats induced precocious puberty as judged by occurrence of vaginal opening, the degree of uterine hypertrophy, changes in ovarian steroid content and incidence of first ovulation. Three types of responses were observed: (I) pubertal ovulation within 96 h; (II) pubertal ovulation within 120 h, and (III) vaginal opening at 120 h not followed by ovulation. All treated animals showed a sustained increase in the LH/FSH ratio in both pituitary and plasma. Plasma estrogen was also increased 1 h after stimulation. A preovulatory rise in plasma estrogen and gonadotropins was noted in type I and type II animals. These data lend further support to the suggestion that brain stimulation causes a release of gonadotrophins which induced ovarian steroidogenesis leading to an ovulatory gonadotropin surge via a positive feedback effect. Changes in pituitary and plasma gonadotropins and plasma estrogen following a unilaeral basic hypothalamic lesion in immature (21-day-old) Sprague-Dawley female rats are described. On Day 23 of life, unilateral electrochemical stimulation of the basal hypothalmus was done. Precocious puberty was thus induced. Pubertal ovulation occurred in 96 or 120 hours or the vaginal opening was noted at 120 hours without ovulation. All treated animals showed a sustained increase in the luteinizing hormone:follicle stimulating hormone (LH:FSH) ratio in both pituitary tissue and plasma. Pituitary FSH remained the same in all 3 groups. Plasma LH and plasma estrogen were increased 1 hour after stimulation and maintained over the next 2 days. A preovulatory rise in plasma estrogen and gonadotropins was noted only when ovulation followed. Hormonal profiles observed suggest that LH-releasing hormone initially discharged from the lesion site activated ovarian estrogenic production which modulated pituitary function. During spontaneous sexual maturation it is thought that other hormones also are factors in the gonadotropin output.
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