Abstract
The acquisition of active avoidance response was studied in 45 to 50-day old rats exposed to ethanol during pregnancy. The offsprings showed no retardation in somatic development although there was a marked deficit in learning of avoidance response. Daily administration of 1-desamino-D-arginine vasopressin (0.1 to 5 micrograms/100 g b.w.), ACTH 4-10 (0.1 to 2 micrograms/100 g b.w.) and adrenaline (0.2 to 2.0 micrograms/100 g b.w.) facilitated the learning performance in a dose-dependent manner. The retention of responding was tested after the interruption of training for 7 days. The prenatally ethanol-exposed rats with DDAVP pretreatment during the 5-day training procedure showed a better performance than that of the vehicle-treated ethanol-exposed rats but they were inferior to the controls. The present data indicate a complexity of biochemical changes due to the prenatal exposure to ethanol and the learning deficit can be modified by either neuropeptides or catecholamines, by such humoral mediators which are known to influence learning behavior and memory consolidation under different experimental conditions and due to different noxious stimuli from noxious stimuli from either external or internal environment.
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