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Prenatal antagonism of stress by naltrexone administration: Early and long‐lasting effects on emotional behaviors in mice
Author(s) -
D'Amato F. R.,
Castellano C.,
AmmassariTeule M.,
Oliverio A.
Publication year - 1988
Publication title -
developmental psychobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 93
eISSN - 1098-2302
pISSN - 0012-1630
DOI - 10.1002/dev.420210309
Subject(s) - naltrexone , psychology , offspring , ontogeny , developmental psychology , context (archaeology) , emotionality , pregnancy , endocrinology , medicine , opioid , biology , paleontology , receptor , genetics
The effects of prenatal exposure to stress and to naltrexone on emotional behaviors were studied in CD1 mice during ontogeny and in the adulthood. During ontogeny (a) lower body weights were initially found in pups born by mothers injected with naltrexone; (b) treatments did not affect sensory motor development except in the case of the cliff aversion reflex which occurred earlier in pups prenatally exposed to stress; (c) measures of ultrasonic vocalizations in stressful context showed that the amount of vocalizations emitted by pups born by stressed mothers was significantly higher than that emitted by pups born by naltrexone injected and control mothers (d) an examination of motheroffspring interactions on the very first day of observation indicated a consistent trend in stressed mothers to be more responsive to their pups. In adulthood, ultrasonic calls in courtship after short and long periods of isolation showed a time‐dependent decrease of vocalizations in males prenatally exposed to naltrexone. These results indicate that the modifications of emotionality evident during early development are directly related to the reactivity of the mothers to the experimental treatments. Moreover, the long‐term reduction of ultrasonic vocalizations in adult males prenatally exposed to naltrexone shows in these animals a lowered reactivity to stressful contexts which probably results from specific physiological alterations due to the prenatal administration of the opiate antagonist.