Each litter was assigned to three treatment groups: handled controls (Han), saline injected animals (Veh), and Dex-treated animals (Dex). All pups within each litter were removed from their mother and treated or handled for a period of five minutes. Animals in the dex group received an intramuscular injection of dex in tapering doses on PD 3 through PD 6. Animals in the Veh group received equivalent volumes of intramuscular sterile saline as the dex animals, and animals in the Han group received no injection but were handled during the same time period on PD 3 through 6. The animals were monitored for:
Measurements. Weight and length were recorded before handling or injection on PD 3-6, 8, 14, and 20 for each treatment group.
Behavioral testing: On PD 21, open-field behavior was assessed.
Adrenocortical response to novelty stress. On PD 33, blood sampling was performed via the tail nick method at 15, 30, 60, and 120 min following exposure to the preference box, with a basal time point obtained before the procedure.
Brain weights. Brain weights were obtained during necropsy on PD 8, 23, and 35.
Body weight, length, rate of growth, brain weight, hormonal values, and behavioral data were averaged across treatment groups.
Results
Somatic (skeletal) growth and brain weight was decreased in dexamethasone-treated animals. Dexamethasone-treated animals also demonstrated delays in gross neurological development on PD 7 and 14 but not PD 20. In late adolescence (PD 33), dexamethasone-treated animals were less active in light and dark environments, while demonstrating a blunted serum corticosterone (the principal glucocortoid in the rat) response to a novel stress.
Conclusions
Given that adequate glucocorticoid activation is vital for learning memory acquisition and is dependent on optimal exposure to elevated glucocorticoid levels, the result
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Contact: Donna Krupa
djkrupa1@aol.com
703-527-7357
American Physiological Society
12-Feb-2002