Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0848255 (female puberty)
 121 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experiments were performed in rats to study the role played by ovarian estrogens, the hypothalamus, the medicortical amygdala, and the ventral hipopcampus in the neurohormonal control of female sexual maturation. The results obtained demonstrated that the ovulation-inducing effect of a single administration of estradiol benzoate (EB) to immature female rats is not tantamount to the induction of precocious puberty. Long-term treatment with very low doses of EB, however, can accelerate sexual maturation, although it was established that the endogenous ovarian estrogen secretion during prepuberal life is not essential for the maturation of the cyclic ovarian function. Implantation of very low quantities of EB into the mediobasal hypothalamus of ovariectomized immature and postpuberal female rats revealed that the hypothalamic sensitivity to the LH-inhibiting effect of estrogen exhibits a gradual decrease that begins some days prior to the onset of puberty. It may be responsible for a temporary elevation of the LH level in the blood triggering final maturation of the ovarian follicles and an increase of estrogen secretion. - Studies on the influence of the limbic system on female sexual maturation lead to the following conclusions: 1. The mediocortical amygdala has an essential function in the maturation of the positive estrogen feedback. 2. An LH-inhibiting activity not related to the negative estrogen feedback is exerted by this nuclear region during critical periods of sexual maturation. It may form an additional protective mechanism against precocious stimulation of the ovaries. 3. By means of its stimulatory action on growth hormone and FSH secretion, the ventral hippocampus may be involved, by cholinergic mechanisms, in the interrelationships between metabolism and the onset of female puberty. The results which suggest a significant role of the limbic system in the control of female sexual maturation will be discussed with regard to recent data obtained in girls and women.
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PMID:Experimental studies on the neurohormonal control of female puberty. 53 37

Activation of LH-releasing hormone (LHRH) secretion, essential for the initiation of puberty, is brought about by the interaction of neurotransmitters and astroglia-derived substances. One of these substances, transforming growth factor alpha (TGFalpha), has been implicated as a facilitatory component of the glia-to-neuron signaling process controlling the onset of female puberty in rodents and nonhuman primates. Hypothalamic hamartomas (HH) are tumors frequently associated with precocious puberty in humans. The detection of LHRH-containing neurons in some hamartomas has led to the concept that hamartomas advance puberty because they contain an ectopic LHRH pulse generator. Examination of two HH associated with female sexual precocity revealed that neither tumor had LHRH neurons, but both contained astroglial cells expressing TGFalpha and its receptor. Thus, some HH may induce precocious puberty, not by secreting LHRH, but via the production of trophic factors--such as TGFalpha--able to activate the normal LHRH neuronal network in the patient's hypothalamus.
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PMID:Some hypothalamic hamartomas contain transforming growth factor alpha, a puberty-inducing growth factor, but not luteinizing hormone-releasing hormone neurons. 1059 38

Manganese (Mn), an essential element considered important for normal growth and reproduction, has been shown in adults to be detrimental to reproductive function when elevated. Because Mn can cross the blood-brain barrier and accumulate in the hypothalamus, and because it has been suggested that infants and children are potentially more sensitive to Mn than adults, we wanted to determine the effects of Mn exposure on puberty-related hormones and the onset of female puberty. We demonstrated that MnCl(2) when administered acutely into the third ventricle of the brain acts dose-dependently to stimulate luteinizing hormone (LH) release in prepubertal female rats. Incubation of hypothalami in vitro showed that this effect was due to a Mn-induced stimulation of luteinizing hormone releasing hormone (LHRH). Further demonstration that this is a hypothalamic site of action was shown by in vivo blockade of LHRH receptors and lack of a direct pituitary action of Mn to stimulate LH in vitro. To assess potential short-term effects, animals were supplemented with MnCl(2) (10 mg/kg) by gastric gavage from day 12 until day 29, or, in other animals, until vaginal opening (VO). Mn caused elevated serum levels of LH, follicle stimulating hormone, and estradiol, and it initiated a moderate but significant advancement in age at VO. Our results are the first to show that Mn can stimulate specific puberty-related hormones and suggest that it may facilitate the normal onset of puberty. They also suggest that Mn may contribute to precocious puberty if an individual is exposed to elevated levels of Mn too early in development.
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PMID:Manganese acts centrally to stimulate luteinizing hormone secretion: a potential influence on female pubertal development. 1574 10