This Article Full Text Full Text (PDF) 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 Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Cohen, P. E. Articles by Pollard, J. W. Search for Related Content PubMed PubMed Citation Articles by Cohen, P. E. Articles by Pollard, J. W.

Colony-Stimulating Factor 1 Regulation of Neuroendocrine Pathways that Control Gonadal Function in Mice

Center for the Study of Reproductive Biology and Women’s Health (P.E.C., L.Z., K.N., J.W.P.), Departments of Developmental and Molecular Biology and Obstetrics and Gynecology and Women’s Health (P.E.C., J.W.P.), Albert Einstein College of Medicine, Bronx, New York 10461

Address all correspondence and requests for reprints to: Jeffrey W. Pollard, Ph.D., Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, New York 10461. E-mail: . pollard{at}aecom.yu.edu

Colony stimulating factor 1 (CSF-1) is the primary regulator of cells of the mononuclear phagocytic lineage. Consequently mice lacking CSF-1 (Csf1^op/Csf1^op) have depleted populations of macrophages in many tissues. In addition, both sexes have reduced fertility with females having extended estrus cycles and poor ovulation rates, whereas males have low circulating LH and T. In this study, we show that puberty was significantly delayed in Csf1^op/Csf1^op females compared with control littermates. Restoration of circulating CSF-1 over the first 2 wk of life accelerated puberty, and this treatment until puberty completely corrected the extended estrous cycles. In a standard LH surge induction protocol, Csf1^op/Csf1^op females showed diminutive negative and no positive feedback response to E2. These data, together with that from male Csf1^op/Csf1^op mice that showed normal release of LH with a GnRH agonist, indicate that the hypothalamus is the site of the primary defect causing fertility problems in CSF-1-deficient mice. In the hypothalamus, microglia are the only CSF-1 receptor-bearing cells, and the recruitment of a full complement these cells is slightly delayed in Csf1^op/Csf1^op mice. These data suggest a role for CSF-1 and its target cells, microglia, in establishing the feedback sensitivity to circulating steroid hormones in the hypothalamus of mice.

This article has been cited by other articles:

				W. V. Ingman and R. L. Jones Cytokine knockouts in reproduction: the use of gene ablation to dissect roles of cytokines in reproductive biology Hum. Reprod. Update, March 1, 2008; 14(2): 179 - 192. [Abstract] [Full Text] [PDF]

				W. V. Ingman, R. L. Robker, K. Woittiez, and S. A. Robertson Null Mutation in Transforming Growth Factor {beta}1 Disrupts Ovarian Function and Causes Oocyte Incompetence and Early Embryo Arrest Endocrinology, February 1, 2006; 147(2): 835 - 845. [Abstract] [Full Text] [PDF]

				R. Wu, K. H. Van der Hoek, N. K. Ryan, R. J. Norman, and R. L. Robker Macrophage contributions to ovarian function Hum. Reprod. Update, March 1, 2004; 10(2): 119 - 133. [Abstract] [Full Text] [PDF]