Neurotrophic factors and female sexual development

Sergio Ojeda, Gregory Dissen, Marie Pierre Junier

    Research output: Contribution to journalArticle

    55 Citations (Scopus)

    Abstract

    Summary: The concept is proposed that polypeptide neurotrophic factors contribute to the developmental regulation of ovarian and hypothalamic function in mammals. Nerve growth factor (NGF) and neurotrophin-3, two members of the neurotrophin family, have been identified in the rat ovary and one of its receptors has been localized to the innervation and thecal cells of developing follicles. Although NGF supports the sympathetic innervation of the gland, the extent to which follicles are innervated appears to be defined by the differential expression of NGF receptors in the theca of developing follicles. The presence of NGF receptors in steroid-producing cells suggests a direct involvement of neurotrophins in the regulation of gonadal endocrine function. Evidence is beginning to emerge suggesting that development of the reproductive hypothalamus is affected by insulin-like growth factor 1 secreted by peripheral tissues, and transforming growth factor α (TGFα) produced locally. In the rat hypothalamus, TGFα appears to be synthesized in both neurons and glial cells. In glial cells it may interact with epidermal growth factor (EGF) receptors to further enhance TGFα synthesis and to, perhaps, stimulate eicosanoid formation. In turn, one of these eicosanoids, prostaglandin E2, may act on luteinizing hormone-releasing hormone (LHRH) neurons to stimulate the release of LHRH in a genomic-independent manner. This provides the basis for the notion that during development LHRH secretion is regulated by a dual mechanism, one that involves transsynaptic effects exerted by neurotransmitters, the other that requires a glial-neuronal interaction and that may predominantly regulate release of the neuropeptide. An increased expression of the TGFα and EGF receptor genes in reactive astrocytes is postulated to contribute to the process by which hypothalamic injury causes sexual precocity. Morphological maturation of the reproductive hypothalamus is thought to occur during sexual development. The process is accelerated by estradiol, which exerts its neurotrophic effects by enhancing the expression of genes encoding cytoskeletal proteins involved in neuronal development and regeneration. It is suggested that acquisition of functional competence by both the ovaries and the reproductive hypothalamus requires the participation of specific, but not similar, neurotrophic factors. The relevance of these concepts to the process of sexual development in other species, particularly primates, remains to be defined.

    Original languageEnglish (US)
    Pages (from-to)120-162
    Number of pages43
    JournalFrontiers in Neuroendocrinology
    Volume13
    Issue number2
    StatePublished - 1992

    Fingerprint

    Sexual Development
    Nerve Growth Factors
    Transforming Growth Factors
    Hypothalamus
    Gonadotropin-Releasing Hormone
    Neuroglia
    Nerve Growth Factor Receptors
    Eicosanoids
    Nerve Growth Factor
    Ovary
    Neurotrophin 3
    erbB-1 Genes
    Neurons
    Cytoskeletal Proteins
    Somatomedins
    Neuropeptides
    Dinoprostone
    Astrocytes
    Mental Competency
    Primates

    Keywords

    • Development, sexual
    • Growth factors
    • Neurotrophins

    ASJC Scopus subject areas

    • Endocrinology, Diabetes and Metabolism
    • Endocrine and Autonomic Systems

    Cite this

    Neurotrophic factors and female sexual development. / Ojeda, Sergio; Dissen, Gregory; Junier, Marie Pierre.

    In: Frontiers in Neuroendocrinology, Vol. 13, No. 2, 1992, p. 120-162.

    Research output: Contribution to journalArticle

    Ojeda, S, Dissen, G & Junier, MP 1992, 'Neurotrophic factors and female sexual development', Frontiers in Neuroendocrinology, vol. 13, no. 2, pp. 120-162.
    Ojeda, Sergio ; Dissen, Gregory ; Junier, Marie Pierre. / Neurotrophic factors and female sexual development. In: Frontiers in Neuroendocrinology. 1992 ; Vol. 13, No. 2. pp. 120-162.
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