Glial-neuronal interactions in the neuroendocrine control of mammalian puberty: Facilitatory effects of gonadal steroids

Sergio Ojeda, Ying J. Ma

    Research output: Contribution to journalArticle

    58 Citations (Scopus)

    Abstract

    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-α (TGFα) 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 E2 (PGE2), 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 (TGFα), (b) increase expression of at least two of the receptors (erbB-4 and erbB-2), and (c) enhance the LHRH response to PGE2 by up-regulating in LHRH neurons the expression of specific PGE2 receptor isoforms. Focal overexpression of TGFα in either the median eminence or preoptic area of the hypothalamus accelerates puberty. Conversely, blockade of either TGFα or NRG hypothalamic actions delays the process. Thus, both TGFα 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.

    Original languageEnglish (US)
    Pages (from-to)528-540
    Number of pages13
    JournalJournal of Neurobiology
    Volume40
    Issue number4
    DOIs
    StatePublished - Sep 15 1999

    Fingerprint

    Puberty
    Gonadotropin-Releasing Hormone
    Neuroglia
    Neuregulins
    Steroids
    Transforming Growth Factors
    Astrocytes
    Neurons
    Dinoprostone
    Hypothalamus
    ErbB-2 Receptor
    Prostaglandin Receptors
    LHRH Receptors
    Median Eminence
    Transforming Growth Factor alpha
    Sexual Development
    Preoptic Area
    Growth Factor Receptors
    Protein-Serine-Threonine Kinases
    Receptor Protein-Tyrosine Kinases

    Keywords

    • Female sexual development
    • Glial growth factors
    • Gonadal steroids
    • Hypothalamic astrocytes
    • Neuroendocrine neurons

    ASJC Scopus subject areas

    • Neuroscience(all)

    Cite this

    Glial-neuronal interactions in the neuroendocrine control of mammalian puberty : Facilitatory effects of gonadal steroids. / Ojeda, Sergio; Ma, Ying J.

    In: Journal of Neurobiology, Vol. 40, No. 4, 15.09.1999, p. 528-540.

    Research output: Contribution to journalArticle

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