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Effects of maternal deprivation on the ACTH stress response in the infant rat
D Suchecki1, D Mozaffarian, G Gross
1Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, CA 94305.
Insights
Maternal deprivation in early life increases stress hormone responses in pups. This study shows deprived pups have higher adrenocorticotropic hormone (ACTH) levels, indicating impaired stress regulation.
Area of Science:
- Neuroscience
- Endocrinology
- Developmental Biology
Background:
- Prolonged maternal deprivation during early development is linked to altered stress responses.
- Elevated basal and stress-induced corticosterone levels are observed in maternally deprived individuals.
Purpose of the Study:
- To investigate if increased adrenocorticotropic hormone (ACTH) secretion contributes to heightened stress responses following maternal deprivation.
- To examine the age-dependent changes in ACTH response to stress in maternally deprived pups.
Main Methods:
- Measurement of ACTH levels in 6-, 9-, and 12-day-old maternally deprived and non-deprived rat pups.
- Exposure of pups to a mild stressor (saline injection and novel environment).
- Assessment of novelty and body heat loss as potential factors influencing ACTH response persistence.
Main Results:
- Maternally deprived pups exhibited a significantly greater ACTH response to saline injection compared to non-deprived pups.
- The magnitude of the ACTH response to stress increased with age in pups.
- Elevated ACTH levels persisted for at least 30 minutes post-stress, independent of novelty or heat loss.
Conclusions:
- Maternal factors play a role in regulating the ACTH response to stress in early development.
- The prolonged ACTH elevation suggests an immature negative feedback system in stressed infant mammals.
Abstract:
Prolonged maternal deprivation during early ontogeny results in increased basal and stress-induced corticosterone levels. In the following experiments we examined whether these increases were due, at least in part, to augmented ACTH secretion. Thus, ACTH levels were measured in 24-hour maternally deprived and nondeprived 6-, 9-, and 12-day-old pups exposed to a mild stressor (i.e. saline injection followed by placement in a novel environment at room temperature). The results showed: (1) nondeprived pups showed a small response to saline--the response of deprived pups, however, was greater than that of nondeprived pups; (2) the magnitude of the response increased with age; (3) ACTH levels remained elevated for at least 30 min. Subsequent experiments examined whether the continuous exposure to novelty and/or loss of body heat could explain the persistence of this response. Neither variable affected the ACTH response to saline. Our results indicate that factors of maternal origin are partly responsible for the regulation of the ACTH response to stress. Furthermore, the persistence of the response suggests that the negative feedback system in the infant is immature.