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.
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.
Mitchell
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V
INSERM U422, Neuroendocrinology and Neuronal Physiopathology, Lille, France. mitchell@lille.inserm.fr
Lecompte
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Beauvillain
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JC
D000818:Animals; D004958:Estradiol / Q000502:physiology*; D047628:Estrogen Receptor alpha; D030762:Estrous Cycle / Q000502:physiology; D005260:Female; D007987:Gonadotropin-Releasing Hormone / Q000502:physiology; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D010052:Ovariectomy; D011301:Preoptic Area / Q000378:metabolism*; D011374:Progesterone / Q000502:physiology*; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017208:Rats, Wistar; D044091:Receptor, Galanin, Type 1 / Q000235:genetics / Q000378:metabolism*; D011960:Receptors, Estrogen / Q000235:genetics / Q000378:metabolism*
D047628:Estrogen Receptor alpha; D012333:RNA, Messenger; D044091:Receptor, Galanin, Type 1; D011960:Receptors, Estrogen; D007987:Gonadotropin-Releasing Hormone; D011374:Progesterone; D004958:Estradiol