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Query: UMLS:C0848255 (female puberty)
 121 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In recent years evidence has begun to accumulate indicating that the central control of mammalian puberty requires not only changes in transsynaptic communication, but also the participation of glial cells. Neurons and astrocytes control the pubertal process by regulating the secretory activity of those neurons that produce luteinizing hormone-releasing hormone (LHRH), the neuropeptide that governs sexual development. LHRH, in turn, directs sexual development by stimulating the secretion of pituitary gonadotropins. Astrocytes affect LHRH neuronal function via cell-cell signaling mechanisms involving several growth factors acting via receptors endowed with tyrosine kinase activity. We have identified two members of the epidermal growth factor/transforming growth factor alpha (EGF/TGFalpha) family and their respective receptors as key players in the glial-neuronal interactive process that regulates LHRH secretion. Our results indicate that TGFalpha and its distant congener neuregulin (NRG) are produced in hypothalamic astrocytes and stimulate LHRH release indirectly via activation of their respective receptors, located--surprisingly--not on LHRH neurons, but on astrocytes. Activation of EGF receptors by TGFalpha, and/or the erbB2/erbB4 receptor complex by NRG, leads to glial release of prostaglandin (PG) E2, which then acts directly on LHRH neurons to stimulate LHRH release. That a central blockade of TGFalpha or NRG action delays puberty, and focal overexpression of TGFalpha advances it, leads to the conclusion that both TGFalpha and NRG are physiological components of the central mechanism controlling the initiation of female puberty.
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PMID:Epidermal growth factor tyrosine kinase receptors and the neuroendocrine control of mammalian puberty. 972 76

It is now clear that astroglial cells actively contribute to both the generation and flow of information within the central nervous system. In the hypothalamus, astrocytes regulate the secretory activity of neuroendocrine neurons. A small subset of these neurons secrete luteinizing hormone-releasing hormone (LHRH), a neuropeptide essential for sexual development and adult reproductive function. Astrocytes stimulate LHRH secretion via cell-cell signaling mechanisms involving growth factors recognized by receptors with either serine/threonine or tyrosine kinase activity. Two members of the epidermal growth factor (EGF) family and their respective tyrosine kinase receptors appear to play key roles in this regulatory process. Transforming growth factor-alpha (TGFalpha) and its distant congeners, the neuregulins (NRGs), are produced in hypothalamic astrocytes. They stimulate LHRH secretion indirectly, via activation of erbB-1/erbB-2 and erbB-4/erbB-2 receptor complexes also located on astrocytes. Activation of these receptors leads to release of prostaglandin E(2) (PGE(2)), which then binds to specific receptors on LHRH neurons to elicit LHRH secretion. Gonadal steroids facilitate this glia-to-neuron communication process by acting at three different steps along the signaling pathway. They (a) increase astrocytic gene expression of at least one of the EGF-related ligands (TGFalpha), (b) increase expression of at least two of the receptors (erbB-4 and erbB-2), and (c) enhance the LHRH response to PGE(2) by up-regulating in LHRH neurons the expression of specific PGE(2) receptor isoforms. Focal overexpression of TGFalpha in either the median eminence or preoptic area of the hypothalamus accelerates puberty. Conversely, blockade of either TGFalpha or NRG hypothalamic actions delays the process. Thus, both TGFalpha and NRGs appear to be physiological components of the central neuroendocrine mechanism controlling the initiation of female puberty. By facilitating growth factor signaling pathways in the hypothalamus, ovarian steroids accelerate the pace and progression of the pubertal process.
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PMID:Glial-neuronal interactions in the neuroendocrine control of mammalian puberty: facilitatory effects of gonadal steroids. 1045 54