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Developmental Changes in Galanin Receptors in the Quail Oviduct and the Effect of Ovarian Sex Steroids on Galanin Receptor Induction¹

Faculty of Integrated Arts and Sciences (K.T., D.L., K.U.), Hiroshima University, Higashi-Hiroshima 739-8521, Japan; and the Department of Biology (M.K., S.I.), Waseda University, Nishi-Waseda 169–50, Japan

Address all correspondence and requests for reprints to: Dr. Kazuyoshi Tsutsui, Faculty of Integrated Arts and Sciences, Hiroshima University, Higashi-Hiroshima 739-8521, Japan. E-mail: tsutsui{at}ue.ipc.hiroshima-u.ac.jp

We have recently isolated an oviposition-inducing peptide from mature quail oviducts identified as avian galanin. This peptide evoked vigorous contractions of the uterine oviduct through binding to receptors located in the uterus. The questions arising from these findings are: what changes occur in galanin receptors in the uterus during maturation, and what is the hormonal factor(s) that induces uterine galanin receptors? Therefore, the present study examined changes in uterine galanin receptors with age and the effect of administration of ovarian sex steroids on galanin receptors in the quail. Immature females reared under long day (LD) photoperiods from 4 weeks of age demonstrated a progressive increase in specific galanin binding per both unit uterine weight and per whole uterus concurrent with uterine development during 4–13 weeks. Scatchard plot analyses of the binding to the uterine preparation showed that the equilibrium dissociation constant (K_d) was about 0.30–0.34 nM regardless of age, and the change in galanin binding during uterine development was due to a change in the number of binding sites. Plasma 17ß-estradiol and progesterone concentrations were almost constant between 4–6 weeks and tended to increase thereafter. Administration of 17ß-estradiol to immature females for 1 week increased not only uterine weight but also specific galanin binding per unit uterine weight, whereas progesterone increased only the binding per unit uterine weight. Both sex steroids also induced an increase in total binding per uterus. Combined administration of 17ß-estradiol and progesterone induced marked increases in the galanin binding, and the effect was not additive but, rather, was synergistic. Scatchard plot analysis showed that the number of binding sites, but not the K_d, was increased by steroid treatment. Administration of 17ß-estradiol or progesterone increased each circulating steroid level to that relatively similar to the maximal levels observed in females exposed to LD.

Thus, ovarian sex steroids may contribute at least in part as hormonal factors to galanin receptor induction, which takes place in the uterine oviduct during development.

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