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Orphanin FQ/nociceptin is a physiological regulator of prolactin secretion in female rats.

Orphanin FQ/nociceptin is a physiological regulator of prolactin secretion in female rats. Research Abstract Details 

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  • Orphanin FQ/nociceptin is a physiological regulator of prolactin secretion in female rats. Abstract Text:

    matthew chesterfieldMatthew Chesterfield,james janikJames Janik,emily murphreeEmily Murphree,courtney lynnCourtney Lynn,erin schmidtErin Schmidt,phyllis callahanPhyllis Callahan,

    Orphanin FQ/nociceptin (OFQ/N), the most recently identified endogenous opioid peptide, stimulates prolactin secretion in both male and female rats. OFQ/N, however, did not elicit this stimulatory effect through the mu-, delta-, or kappa-opiate receptor subtype. The role OFQ/N plays in prolactin regulation under physiological conditions and its mechanism of action are not known. The purpose of these studies was to determine the physiological significance and pharmacological specificity of the prolactin secretory response to OFQ/N. In addition, the role of the tuberoinfundibular dopaminergic (TIDA) neurons in mediating this response was examined. Opioid receptor-like-1 (ORL-1) receptors were blocked by pretreatment with compound B (Comp B), a purported OFQ/N antagonist, or receptor synthesis was disrupted by pretreatment with ORL-1 receptor antisense oligonucleotides. The prolactin secretory response to OFQ/N administration in diestrous females was measured. Furthermore, the suckling-induced prolactin response was also determined after Comp B pretreatment. TIDA neuronal activity was quantified in diestrous female rats to determine whether OFQ/N stimulates prolactin release by inhibiting TIDA neurons. OFQ/N significantly inhibited the TIDA neurons by 1 min, preceding the prolactin secretory response. Both Comp B and antisense pretreatment blocked the stimulatory effects of OFQ/N on prolactin release, and Comp B abolished the suckling-induced prolactin response. These studies indicate that OFQ/N is a potent stimulus for prolactin secretion in female rats and that it mediates this effect by rapid and transient inhibition of TIDA neuronal activity. Furthermore, OFQ/N plays a physiologically significant role in the regulation of prolactin secretion during lactation, and it mediates its effects via actions at the ORL-1 receptor subtype.

    Orphanin FQ/nociceptin is a physiological regulator of prolactin secretion in female rats. Publishing Authors By Initials

    m chesterfieldM Chesterfield,j janikJ Janik,e murphreeE Murphree,c lynnC Lynn,e schmidtE Schmidt,p callahanP Callahan,

    For similar proteins: membrane proteins: receptors, cell surface: receptors, g-protein-coupled: receptors, opioid research abstracts see: proteins: membrane proteins: receptors, cell surface: receptors, g-protein-coupled: receptors, opioid research

    PUBMED ID PMID:

    MEDLINE DATE:

    Orphanin FQ/nociceptin is a physiological regulator of prolactin secretion in female rats. Journal Published:

    PUBLICATION TYPE: Research Support, N.I.H., Extr

    Journal: Endocrinology

    VOLUME: 147

    Page Numbers: 5087-93

    Journal Abbreviation: Endocrinology

    ISSN: 0013-7227

    DAY: 3

    MONTH: 08

    YEAR: 2006

    Orphanin FQ/nociceptin is a physiological regulator of prolactin secretion in female rats. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 375040

    Orphanin FQ/nociceptin is a physiological regulator of prolactin secretion in female rats. Keywords Mesh Terms:

    KEYWORDS: Receptors, Opioid

    MESH TERMS: physiology

    Chemical & Substance for Abstract: Orphanin FQ/nociceptin is a physiological regulator of prolactin secretion in female rats. Information

    Substance Name: Prolactin

    Registry Number: 9002-62-4

    Grant and Affiliation Information for Orphanin FQ/nociceptin is a physiological regulator of prolactin secretion in female rats.

    AFFILIATION: Center for Neuroscience, Department of Zoology, Miami University, Oxford, Ohio 45056, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NICHD

    GRANT: HD46479

    ACRONYM: HD

    MEDLINETA: Endocrinology

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

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