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Facilitation of Lordosis in Rats by a Metabolite of Luteinizing Hormone Releasing Hormone

Program in Neuroscience and Department of Obstetrics and Gynecology (T.J.W., S.K.M.), Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814; Midwest Proteome Center and Department of Biochemistry and Molecular Biology (M.J.G.), Rosalind Franklin School of Medicine and Science, Chicago, Illinois 60064; Department of Pharmacology (J.L.R.), The University of Texas Health Science Center, San Antonio, Texas 78229; and Department of Molecular and Cellular Biology, Psychiatry and Behavioral Sciences (S.K.M.), Baylor College of Medicine, Houston, Texas 77030

Address all correspondence and requests for reprints to: T. John Wu, Ph.D., Department of Obstetrics and Gynecology, Room B2020, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, Maryland 20814. E-mail: twu{at}usuhs.mil; or Shaila Mani, Ph.D., Departments of Molecular and Cellular Biology, Psychiatry and Behavioral Sciences, Baylor College of Medicine, Houston, Texas 77005. E-mail: smani{at}bcm.edu.

In the female rat, ovulation is preceded by a marked increase in the release of the decapeptide, LHRH, culminating in a preovulatory LH surge, which coincides with a period of sexual receptivity. The decapeptide, LHRH, is processed by a zinc metalloendopeptidase EC 3.4.24.15 (EP24.15) that cleaves the hormone at the Tyr⁵-Gly⁶ bond. We have previously reported that the autoregulation of LHRH gene expression can also be mediated by its metabolite, LHRH-(1–5). Given the central function of LHRH in reproduction and reproductive behavior, we examined the role of the metabolite, LHRH-(1–5), in mediation of LHRH-facilitated reproductive behavior. Intracerebroventricular administration of LHRH-(1–5) facilitated sexual behavior responses, similar to those facilitated by the decapeptide LHRH, in ovariectomized estradiol-primed female rats. Furthermore, immunoneutralization of EP24.15 resulted in the inhibition of the LHRH-facilitated lordosis but had no inhibitory effects on LHRH-(1–5)-facilitated lordosis. The LHRH antagonist, Antide, was capable of inhibiting LHRH-facilitated lordosis, without affecting LHRH-(1–5)-facilitated lordosis. Collectively, these results suggest a role for LHRH metabolites in the facilitation of female receptive behavior in rats.

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