NOVEL MECHANISMS UNDERLYING THE TRANSSYNAPTIC CONTROL OF LHRH RELEASE

LHRH 释放的跨突触控制的新机制

• 批准号: 8357725
• 负责人: Sergio R Ojeda
• 金额: $ 3.63万
• 依托单位: OREGON HEALTH & SCIENCE UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2011
• 资助国家: 美国
• 起止时间: 2011-05-01 至 2012-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8357725
• 关键词: Adult; Amenorrhea; Communication; Competence; Family; Female; Funding; Genes; Glutamates; Gonadotropin Hormone Releasing Hormone; Grant; Human; Hypothalamic structure; Ion Transport; Kallmann Syndrome; Mediating; National Center for Research Resources; Nature; Neuroglia; Neurons; Periodicity; Play; Primates; Principal Investigator; Proteins; Regulation; Regulatory Element; Reproduction; Research; Research Infrastructure; Resources; Role; Signal Pathway; Source; Synapses; Syndrome; Testing; United States National Institutes of Health; cost; gamma-Aminobutyric Acid; member; novel; reproductive

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. Luteinizing hormone-releasing hormone (LHRH) secretion is controlled by transsynaptic inputs of both excitatory and inhibitory nature, in addition to glia-to-neuron signaling pathways. Neurons that utilize gamma aminobutyric acid (GABA) for synaptic communication provide the major inhibitory input to the LHRH neuronal network. We have conducted studies to define the impact that these regulatory components may exert on the functional competence of LHRH neurons during female adulthood. The hypotheses tested were: 1) that excitatory GABAAR-mediated inputs exerted directly on LHRH neurons are required for normal reproductive cyclicity, 2) that members of the novel FXYD family of ion transport-controlling proteins play in the regulation of LHRH secretion, 3) that Nell2, a novel gene specifically expressed in glutamatergic neurons, is an upstream regulatory element required for the glutamatergic control of reproduction, and 4) that a novel gene known as C14ORF4 plays a role in coordinating the dual excitatory/inhibitory transsynaptic control of reproductive cyclicity. The concepts derived from these studies are expected to increase our understanding of the cellular mechanisms underlying the loss of reproductive competence in human syndromes such as hypothalamic amenorrhea and idiopathic hypothalamic hypogonadism.

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