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Glucocorticoids and parental hyperphagia in ring doves (Streptopelia risoria)
Kristin A Koch1, John C Wingfield, John D Buntin
1Department of Biological Sciences, University of Wisconsin-Milwaukee, Milwaukee, Wisconsin 5320l, USA.
Hormones and Behavior
|February 28, 2002
Summary
Glucocorticoids, like corticosterone, increase food intake in parent doves, supporting parental care. This effect is mediated by the central nervous system, suggesting a role in breeding behaviors.
Area of Science:
- Behavioral Endocrinology
- Neuroscience
Background:
- Parental care in birds involves significant behavioral changes, including increased food consumption.
- Glucocorticoids are stress hormones known to influence various physiological and behavioral processes.
Purpose of the Study:
- To investigate the role of glucocorticoids in mediating increased food consumption during parental care in ring doves.
- To determine if central nervous system (CNS) pathways are involved in the hyperphagic effects of glucocorticoids.
Main Methods:
- Measured plasma corticosterone levels in breeding female ring doves during incubation and posthatching phases.
- Administered intracerebroventricular (icv) injections of dexamethasone (DEX) and the antagonist RU38486 in nonbreeding doves to assess effects on food intake.
- Compared systemic versus icv administration of DEX to localize its action.
Main Results:
- Plasma corticosterone was higher in breeding females posthatching compared to incubation.
- Central administration of DEX significantly increased food intake in both sexes, dose-dependently in males.
- Systemic DEX did not increase feeding, indicating a CNS-mediated effect.
- RU38486 blocked DEX-induced hyperphagia, confirming the involvement of glucocorticoid receptors in the CNS.
Conclusions:
- Corticosterone likely contributes to the increased food consumption (parental hyperphagia) observed in breeding doves.
- The orexigenic (appetite-stimulating) effects of corticosterone appear to be mediated by CNS binding sites similar to mammalian glucocorticoid receptors.