Articles by Kellie M. Breen in JoVE
Frequent Tail-tip Blood Sampling in Mice for the Assessment of Pulsatile Luteinizing Hormone Secretion Richard B. McCosh1, Michael J. Kreisman1, Kellie M. Breen1 1Department of Reproductive Medicine, University of California, San Diego School of Medicine Here we present a tail-tip blood sampling protocol for frequent sample collection in unrestrained mice. This method is useful for assessing patterns of pulsatile luteinizing hormone secretion and could be adapted for analysis of other circulating factors.
Other articles by Kellie M. Breen on PubMed
Insight into the Neuroendocrine Site and Cellular Mechanism by Which Cortisol Suppresses Pituitary Responsiveness to Gonadotropin-releasing Hormone Endocrinology. Feb, 2008 | Pubmed ID: 17962347 Stress-like elevations in plasma glucocorticoids rapidly inhibit pulsatile LH secretion in ovariectomized sheep by reducing pituitary responsiveness to GnRH. This effect can be blocked by a nonspecific antagonist of the type II glucocorticoid receptor (GR) RU486. A series of experiments was conducted to strengthen the evidence for a mediatory role of the type II GR and to investigate the neuroendocrine site and cellular mechanism underlying this inhibitory effect of cortisol. First, we demonstrated that a specific agonist of the type II GR, dexamethasone, mimics the suppressive action of cortisol on pituitary responsiveness to GnRH pulses in ovariectomized ewes. This effect, which became evident within 30 min, documents mediation via the type II GR. We next determined that exposure of cultured ovine pituitary cells to cortisol reduced the LH response to pulse-like delivery of GnRH by 50% within 30 min, indicating a pituitary site of action. Finally, we tested the hypothesis that suppression of pituitary responsiveness to GnRH in ovariectomized ewes is due to reduced tissue concentrations of GnRH receptor. Although cortisol blunted the amplitude of GnRH-induced LH pulses within 1-2 h, the amount of GnRH receptor mRNA or protein was not affected over this time frame. Collectively, these observations provide evidence that cortisol acts via the type II GR within the pituitary gland to elicit a rapid decrease in responsiveness to GnRH, independent of changes in expression of the GnRH receptor.
Influence of Stress-induced Intermediates on Gonadotropin Gene Expression in Gonadotrope Cells Molecular and Cellular Endocrinology. Mar, 2014 | Pubmed ID: 24012628 Despite extensive investigation, a comprehensive understanding of the mechanisms whereby stress impacts fertility remains elusive. Since the 1930s, when Hans Selye popularized studying adaptations to stress (Selye, 1937), we have learned that compensatory mechanisms involve a complex interplay of neural and hormonal processes that allow various body functions to adjust to stress, in a coordinated manner. In terms of reproduction, the adjustment to a stressor interferes with integrated functioning at multiple levels of regulation--the hypothalamus, anterior pituitary gland, gonads, and neural centers coordinating behavior. Various mediators are postulated to participate in reproductive suppression. These include catecholamines, cytokines, prostaglandins, endogenous opioid peptides, and hormones of the hypothalamic-pituitary-adrenal axis. This review focuses on one class of mediators, the glucocorticoids, and provides our views on the relevance and mode of action of this inhibitory intermediate within the anterior pituitary gonadotrope, as a potential cellular site whereby glucocorticoids contribute to stress-induced reproductive suppression.