Jill M Weathington

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Corticotropin-releasing factor receptors type 1 (CRF(1)) and type 2 (CRF(2)) have complementary roles in controlling the hypothalamic-pituitary-adrenal (HPA) axis. Because CRF receptors are expressed in sex steroid-sensitive areas of the forebrain, they may contribute to sex-specific patterns of stress sensitivity and susceptibility to stress-related mood(More)
To compare the response of the medial amygdala and central amygdala to juvenile social subjugation (JSS), we used unbiased stereology to quantify the immediate early gene product Fos in prepubertal rats after aggressive or benign social encounters or handling. We estimated the overall number of neurons and the proportion of Fos immunoreactive neurons in the(More)
After experiencing juvenile social subjugation (JSS), adult female rats display more severe depression- and anxiety-like behaviors than adult males, suggesting that JSS is encoded in a sex-specific manner. To test this hypothesis, prepubertal rats (P28-33) were subjected to 10 aggressive acts in ≤10 min from an aggressive adult male, a 10 min encounter with(More)
One of the most reliable findings in psychiatry is in the incidence of anxiety and depression. Beginning at puberty, women develop mood disorders twice as often as men. Because corticotropin-releasing factor (CRF) receptors are implicated, we compared CRF receptor binding in pre- and postpubertal rats. In each brain area, CRF receptor binding was sexually(More)
Child abuse is the most significant environmental risk factor for the development of mood disorders, which occur twice as frequently in women as in men. To determine whether juvenile social subjugation (JSS) of rats induces mood disorder-like symptoms, we exposed 28 day-old male and female rats to daily aggressive acts from aggressive male residents. Each(More)
Child abuse is the most potent experiential risk factor for developing a mood disorder later in life. The effects of child abuse are also more severe in girls and women than in men. In this review, we explore the origins of this epidemiological sex difference. We begin by offering the hypothesis that a sex-specific risk factor that influences how social(More)
Many of the best-studied neural sex differences relate to differences in cell number and are due to the hormonal control of developmental cell death. However, several prominent neural sex differences persist even if cell death is eliminated. We hypothesized that these may reflect cell phenotype "decisions" that depend on epigenetic mechanisms, such as DNA(More)
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