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Previous Article | Next Article
Volume 16, Number 12, Issue of June 15, 1996 pp. 3943-3949
Copyright ©1996 Society for NeuroscienceMaternal Glucocorticoid Secretion Mediates Long-Term Effects of Prenatal Stress
Received Jan. 11, 1996; revised April 2, 1996; accepted April 3, 1996.
Arnaud Barbazanges, Pier Vincenzo Piazza, Michel Le Moal, and Stefania Maccari Psychobiologie des Comportements Adaptatifs, INSERM U259, Université de Bordeaux II, Domaine de Carreire, 33077 Bordeaux Cedex, France
There is growing evidence that stressors occurring during pregnancy can impair biological and behavioral adaptation to stress in the adult offspring. Mechanisms by which stress in the pregnant rat can influence development of the offspring are still unknown. In the present study, we investigated the involvement of maternal corticosterone secretion during pregnancy on the hypothalamo-pituitary-adrenal axis activity of adult offspring. We investigated stress-induced corticosterone secretion and hippocampal type I and type II corticosteroid receptors in male adult rats submitted to prenatal stress born to either mothers with intact corticosterone secretion or mothers in which stress-induced corticosterone secretion was blocked by adrenalectomy with substitutive corticosterone therapy. Repeated restraint during the last week of pregnancy was used as prenatal stressor. Furthermore, the specific role of an injection of corticosterone before the restraint stress on adrenalectomized mothers with substitutive corticosterone treatment was also studied. We report here that blockade of the mother's stress-induced glucocorticoid secretion suppresses the prolonged stress-induced corticosteroid response and the decrease in type I hippocampal corticosteroid receptors usually observed in prenatally stressed adults. Conversely, corticosterone administered during stress, to mothers in which corticosterone secretion is blocked, reinstates the effects of prenatal stress. These results suggest for the first time that stress-induced increases in maternal glucocorticoids may be a mechanism by which prenatal stress impairs the development of the adult offspring's glucocorticoid response.
Key words: corticosterone; corticosteroid receptors; hippocampus; prenatal stress; maternal environment; development
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