Regulation of galanin receptor GalR1 mRNA expression by ovarian steroids in oestrogen receptor alpha-immunoreactive neurones: identification of distinct populations of neurones in the preoptic area.

摘要

This study examined whether gonadal steroids are involved in regulating galanin receptor 1 (GalR1) mRNA expression in neurones that contain oestrogen receptor alpha (ERalpha), in three regions of the preoptic area (POA) known to be involved in the control of gonadotropin secretion. Double-labelling immunohistochemistry using an antibody against the ERalpha and in situ hybridization experiments using a 35S-labelled riboprobe specific for GalR1 mRNAs revealed that ERalpha is expressed in a large proportion of GalR1 mRNA-expressing neurones of the POA in the ovariectomized (OVX) female rat. Oestradiol (E2) and oestradiol plus progesterone (E2 + P) treatments of OVX rats significantly decreased the proportion of GalR1 mRNA/ERalpha immunoreactive (ERalpha-IR) neurones in the anteroventral periventricular nucleus (AVPV), medial preoptic nucleus (MPN) and medial preoptic area (MPO). The expression of GalR1 mRNA in ERalpha-IR neurones varied according the hormonal status of the female animals. In the AVPV, during the oestrous cycle, the hybridization signal significantly increased at oestrus. E2 and E2 + P treatments of OVX rats did not induced significant variation of levels of GalR1 mRNAs in ERalpha-IR neurones. In the MPN, E2 treatment of OVX rats resulted in significant increase in GalR1 mRNA expression in ERalpha-IR neurones. Similarly, levels of the GalR1 hybridization signal increased during afternoon of proestrus and oestrus. In the MPO, treatment of OVX rats with E2 + P significantly decreased GalR1 mRNA expression in ERalpha-IR neurones. The expression of GalR1 mRNA did not change during the oestrous cycle in this area. These findings suggest that the hypothalamic action of galanin on gonadotopin-releasing hormone (GnRH) secretion may pass through the specific population of GalR1/ERalpha-IR neurones of the MPN in mediating the oestrogen action on the GnRH system at the moment of the luteinizing hormone surge.