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This Article Full Text Full Text (PDF) All Versions of this Article: 70/2/348    most recent biolreprod.103.020818v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal My Folders Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Zapatero-Caballero, H. Articles by Fernandez-Vazquez, G. Search for Related Content PubMed PubMed Citation Articles by Zapatero-Caballero, H. Articles by Fernandez-Vazquez, G. Agricola Articles by Zapatero-Caballero, H. Articles by Fernandez-Vazquez, G.

Gonadotropin-Releasing Hormone Receptor Gene Expression During Pubertal Development of Female Rats¹

Servicio de Endocrinología,³ Hospital Carlos III, Instituto de Salud Carlos III, 28029 Madrid, Spain Consejo Superior de Investigaciones Cientificas,⁴ 28029 Madrid, Spain

Appropriate expression of the GnRH receptor (GnRH-R) in gonadotrophs is critical for GnRH signaling and hence for gonadotropin secretion and sexual development. In the present work, we have studied the ontogeny of the steady-state GnRH-R mRNA levels in pituitaries of female rats from Day 5 to Day 55, when sexual maturity is attained. Developmental changes of gonadotropin subunit (, FSHß, and LHß) mRNA levels were also assessed. In addition, the role of the endogenous GnRH on the maturational changes of GnRH-R and gonadotropin subunit gene expression was investigated. Messenger RNA levels were determined by Northern blot analysis of total RNA from anterior pituitaries. Amounts of the most abundant (5.0 kilobase [kb]) GnRH-R mRNA increased slowly from Day 5 through the infantile period, to peak at Day 20 (4-fold increase vs. Day 5). Thereafter the levels of the GnRH-R mRNA decline abruptly by Day 25 (75% decrease vs. Day 20) and then fell slightly until Day 35. Parallel changes were observed on the 4.5-kb transcript of the GnRH-R gene. Alpha subunit mRNA was easily detected at Day 5 and its levels increased quickly through the beginning of the infantile period to peak at Day 10 (3.2-fold increase vs. Day 5); then it decreased by 85% at Day 35. FSHß and LHß mRNA levels rose slowly until Days 15–20, a short time before GnRH-R. Thereafter, the levels of both mRNAs fell until Day 35 (90% decrease vs. Day 15 for FSHß and 50% decrease vs. Day 20 for LHß). To ascertain whether developmental activation of the GnRH-R and gonadotropin subunit gene expression is GnRH dependent, we have studied the effect of blocking the endogenous GnRH action by treating developing female rats with the specific GnRH antagonist cetrorelix (1.5 mg/kg body weight/wk, s.c.) through the infantile (Days 5–20) and the juvenile period (Days 20–35). Cetrorelix completely blocked the rise of levels of the two most abundant species, 5.0 kb and 4.5 kb, of GnRH-R mRNA during the infantile phase and dropped them to almost undetectable levels during the juvenile prepubertal period. Cetrorelix also abolished the developmental rise of gonadotropin ß subunit mRNAs during the two periods of the study. In contrast, subunit gene expression tended to decrease, but not significantly, with cetrorelix treatment during the two periods. These data demonstrate that sexual maturation of female rats is advanced by an early and strong induction of GnRH-R and gonadotropin subunit gene expression during the infantile period, followed by weaker persistent activation during puberty. Developmental GnRH-R and gonadotropin ß subunit gene expression is almost entirely GnRH dependent, not only in the juvenile prepubertal stage but also during the infantile period.

¹ Supported by grants PM95-212 from the Ministerio de Educación y Ciencia and 99/0412 from the Fondo de Investigación Sanitaria (to G.F.V.) and by a predoctoral fellowship from the Instituto de Salud Carlos III (to H.Z.C.)

² Correspondence: Gumersindo Fernandez-Vazquez, Servicio de Endocrinología, Hospital Carlos III, Instituto de Salud Carlos III, Sinesio Delgado 10, Madrid 28029, Spain. FAX: 34-91 733 6614; gfernandez.hciii{at}salud.madrid.org

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