Third Pathophysiology of Prenatal Cocaine ExposureLester B.M. · Padbury J.F.
Warren Alpert Medical School of Brown university, Women and Infants’ Hospital of Rhode Island, Providence, R.I., USA
Barry M. Lester, PhD
Women and Infants’ Hospital of Rhode Island
101 Dudley Street
Providence, RI 02905 (USA)
Tel. +1 401 453 7640, Fax +1 401 453 7646, E-Mail Barry_Lester@Brown.edu
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The pathophysiology of the effects of cocaine on fetal development has been described along 2 major pathways: neurochemical effects and vasoconstrictive effects. Following a summary of these effects, we suggest a ‘third pathophysiology’ in which altered fetal programming affects the acute and long-term adverse effects of in utero cocaine exposure. We describe how cocaine as a stressor alters the expression of key candidate genes, increasing exposure to catecholamines and fetal cortisol-altering neuroendocrine (hypothalamic-pituitary-adrenal axis) activity, leading to infant behavioral dysregulation, poor behavioral control and emotion regulation during childhood and phenotypes that confer vulnerability to substance use in adolescence. This model is discussed in relation to follow-up studies of the effects of in utero cocaine exposure and maturational changes in brain development.
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