This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Objective: To characterize the effect of corticotropin-releasing factor in stress-related disruption of primate maternal behavior. Stress can inhibit maternal behavior in humans and other mammals;however, this effect is poorly understood, and the neural and neuroendocrine mechanisms are unknown. To begin to elucidate the mechanisms by which stress can alter maternal behavior in primates, we are conducting a series of experiments investigating the interactions between maternal behavior and stress in marmoset monkeys. Initial results indicate that lactating females may show altered neuroendocrine responses to stress as compared to non-breeding females, including somewhat dampened pituitary secretion of adrenocorticotropic hormone (ACTH) but elevated adrenocortical release of cortisol, resulting in a significantly altered cortisol:ACTH ratio. Second, we have found that neither acute nor chronic treatment with exogenous cortisol markedly affects maternal behavior in experienced mothers, under either baseline or stressful conditions. In contrast, initial findings from an ongoing experiment suggest that direct administration of the neuropeptide corticotropin-releasing factor (CRF) into the brain inhibits maternal responsiveness in lactating females. These results, although preliminary, suggest that stress may disrupt maternal behavior primarily through direct neural effects of CRF rather than through activation of the hypothalamic-pituitary-adrenal endocrine axis. This research used Animal Services and Assay Services. Publications are pending.

Agency
National Institute of Health (NIH)
Institute
National Center for Research Resources (NCRR)
Type
Primate Research Center Grants (P51)
Project #
5P51RR000167-48
Application #
7958766
Study Section
Special Emphasis Panel (ZRR1-CM-8 (01))
Project Start
2009-05-01
Project End
2010-04-30
Budget Start
2009-05-01
Budget End
2010-04-30
Support Year
48
Fiscal Year
2009
Total Cost
$46,835
Indirect Cost
Name
University of Wisconsin Madison
Department
Type
Other Domestic Higher Education
DUNS #
161202122
City
Madison
State
WI
Country
United States
Zip Code
53715
Kang, HyunJun; Mesquitta, Walatta-Tseyon; Jung, Ho Sun et al. (2018) GATA2 Is Dispensable for Specification of Hemogenic Endothelium but Promotes Endothelial-to-Hematopoietic Transition. Stem Cell Reports 11:197-211
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