To the Editor: The quality and safety movement has brought necessary attention to health systems science as a third pillar of medical training alongside the basic and clinical sciences. The American Medical Association's health systems science framework 1 includes advocacy as a key health care process, underscoring the need for physicians to advocate for patients by improving access to care, using community and governmental resources, addressing health disparities, and influencing health policy. However, undergraduate medical education curricula have limited capacity for additional advocacy training. Student-run extracurricular organizations, such as Vanderbilt University School of Medicine's Social Mission Committee, provide an opportunity to fill this gap. The goal of the Social Mission Committee is to advance the social mission of our medical school by empowering students, faculty, and staff to actively partner with our communities to achieve health equity.
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Background: Estrogen increases dramatically during pregnancy, but quickly drops below prepregnancy levels at birth and remains suppressed during the postpartum period. Clinical and rodent work suggests that this postpartum drop in estrogen results in an "estrogen withdrawal" state that is related to changes in affect, mood, and behavior. Most studies examining the effect of estrogen withdrawal on the brain have focused solely on the hippocampus. Methods: We used a hormone-simulated pseudopregnancy model in Syrian hamsters, a first for this species.Ovariectomized females were given daily injections to approximate hormone levels during gestation and then withdrawn from estrogen to simulate postpartum estrogen withdrawal.Subjects were tested for behavioral assays of anxiety and anhedonia during estrogen withdrawal. Following sacrifice, neuroplasticity in oxytocin-producing neurons in the paraventricular nucleus of the hypothalamus (PVH) and its efferent targets was measured.Results: Estrogen-withdrawn females had increased anxiety-like behaviors in the elevated plus and open field, but did not differ from controls in sucrose preference. Furthermore, estrogenwithdrawn females had more oxytocin-immunoreactive cells and oxytocin mRNA in the PVH, as well as an increase in oxytocin receptor density in the dorsal raphe nucleus (DRN). Finally, blocking oxytocin receptors in the DRN during estrogen withdrawal prevented the high-anxiety behavioral phenotype in estrogen-withdrawn females. Conclusions: Estrogen withdrawal alters oxytocin signaling in the PVH and DRN to increase anxiety-like behavior during the postpartum period. More broadly, these experiments suggest Syrian hamsters as a novel organism in which to model the effects of postpartum estrogen withdrawal on the brain and anxiety-like behavior.
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