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Postnatal handling does not attenuate hypothalamic-pituitary-adrenal hyperresponsiveness after prenatal ethanol
1Department of Anatomy, University of British Columbia, Vancouver, Canada.
Alcoholism, Clinical and Experimental Research
|October 25, 2000
Summary
Postnatal handling did not protect against prenatal ethanol exposure's effects on stress responses. Prenatal ethanol exposure caused sex-specific alterations in the hypothalamic-pituitary-adrenal (HPA) axis feedback regulation.
Area of Science:
- Neuroscience
- Endocrinology
- Developmental Psychology
Background:
- Prenatal ethanol exposure leads to heightened hypothalamic-pituitary-adrenal (HPA) axis activity in adult animals.
- Postnatal handling, an early environmental intervention, typically reduces HPA activity throughout life.
- Altered HPA axis feedback regulation may underlie the effects of both prenatal ethanol exposure and postnatal handling.
Purpose of the Study:
- To investigate if postnatal handling can mitigate the effects of prenatal ethanol exposure on HPA axis hormonal responses to stress.
- To examine sex-specific differences in HPA axis regulation following prenatal ethanol exposure and postnatal handling.
Main Methods:
- Male and female Sprague Dawley rats were exposed to ethanol (E), pair-fed (PF), or control (C) conditions prenatally, and were either handled (H) or nonhandled (NH) postnatally.
- At 4-5 months of age, animals were subjected to restraint stress after saline (SAL) or dexamethasone (DEX) administration to assess HPA responsiveness.
- Blood samples were collected to measure adrenocorticotropic hormone (ACTH) and corticosterone (CORT) levels.
Main Results:
- Dexamethasone (DEX) significantly reduced ACTH and corticosterone (CORT) in both sexes, indicating successful blockade of endogenous HPA activity.
- Handled (H) animals exhibited greater suppression of HPA activity compared to nonhandled (NH) animals across prenatal groups.
- Prenatal ethanol-exposed (E) females showed elevated ACTH and CORT even after DEX administration, suggesting impaired feedback, while males showed this only after saline (SAL).
Conclusions:
- Prenatal ethanol exposure induces sex-specific deficits in HPA axis feedback regulation, particularly in females.
- While postnatal handling generally reduces stress responses, it does not attenuate the HPA hyperresponsiveness or feedback impairments caused by prenatal ethanol exposure.
- These findings highlight the lasting impact of early-life ethanol exposure on neuroendocrine stress systems and underscore sex differences in vulnerability.