NIDA Home > About NIDA > Organization > Child & Adolescent Workgroup (CAWG) > Prenatal Drug Exposure and Drug-Abusing Environments  

Child & Adolescent Workgroup (CAWG)
gray line



Prenatal Drug Exposure and Drug-Abusing Environments


Research Findings from September, 2000 Director's Report

This section lists selected summaries from NIDA funded research projects that investigate the consequences of prenatal drug exposure. The summaries provided were selected from recent issues of the Director's Report to the National Advisory Council on Drug Abuse. For a more comprehensive listing of NIDA funded projects see the Director's Report.


In Utero Cocaine Exposure Affects the Respiratory System

Dr. Immanuela Moss and her associates recently reported on the role of endogenous opioid systems, specifically met-enkephalin, in the attenuation of respiration by repeated prenatal cocaine exposure. These investigations were designed to delineate the contribution of met-enkephalin, an endogenous opioid peptide, in the attenuation of cocaine-induced respiratory and arousal responses in six- to seven-day-old and in 20- to 21-day-old piglets. In both age groups, prenatal exposure to cocaine increased met-enkephalin immunoreactivity in the respiratory- and arousal-related medullary regions. These findings support the investigators' hypothesis of a modulatory role of met-enkephalin in the normal development of respiratory control and an involvement of this peptide in the attenuation of respiration by repeated prenatal cocaine exposure. Liu, J-K., Laferriere, A. and Moss, I.R. Brain Research Bulletin. 51, pp. 419-424, 2000.

Prenatal Exposure to Cocaine Can Affect the Outcome of Serotonin Receptor Stimulation in the Brains of the Offspring When They Are Tested As Adults

Dopamine normally inhibits the activity of cholinergic neurons in the striatum, and this inhibition is an important aspect of the control of motor activity. However, the activity of the dopamine-containing neurons is regulated by serotonergic activity at the 5HT3 receptor site, the only serotonin receptor of the 17 identified thus far that is an ion channel. The application of a 5HT3 agonist normally limits the release of acetylcholine in a dose-dependent manner. However, prenatal exposure to cocaine alters this relationship in female, but not in male rats. Denise Jackson and her colleagues treated rat mothers with 20 mg/kg of cocaine or saline solution (the control) twice daily from embryonic days 15 to 21 (day of birth). The rats were tested as adults (postnatal days 80-120). Both males and females (at two times in the estrous cycle) that had been treated with saline in utero showed the expected inhibition of cholinergic activity after graded doses of a 5HT3 agonist were applied to the neurons; however, females in diestrus, a relatively quiescent period during the rodent estrous cycle, were much less sensitive to the lower doses of the agonist. This is important because it demonstrates a functional difference in the brains of females given cocaine prenatally; a difference that is apparent in adulthood. The data also suggest that estrogen may modify the response, as animals in the phase of the cycle when estrogen is high did not display this deficit. This result suggests that persistent modification of the dopaminergic system has occurred as the cholinergic output is altered, and suggests that other parts of the mesocorticolimbic dopamine system may be functionally altered, possibly including regions that control motor activity and the perception of reward. Bolanos, C.A., Trksak, G.H., Glatt, S.J. and Jackson, D. Synapse, 36, pp. 1-11, 2000.

Sex Differences in Language Production in 24-Month-Old Inner City Children Exposed In Utero to Cocaine

Researchers at the Yale Child Study Center compared the language abilities at age 24 months of 47 inner-city children exposed prenatally to cocaine with those of 30 inner-city children not exposed prenatally to cocaine. The sample was recruited prenatally. While both groups of children evidenced some delays in language development, the non-cocaine-exposed children produced more complex language, including longer utterances, a richer vocabulary, and more complex grammatical structure than the cocaine-exposed children were able to do. The effect, however, was largely in girls. Malakoff, M.E., Mayes, L.C., Schottenfeld, R., and Howell, S. Language Production in 24 Month Old Inner City Children Exposed In Utero to Cocaine. Journal of Applied Developmental Psychology, 20, pp. 159-180, 2000.

Maternal Smoking During Pregnancy and Toddler's Negative Behavior

This study extends previous studies by looking at the effect of the mother's smoking during pregnancy on her toddler's negative behavior. A survey consisting of a structured questionnaire was administered to the mothers of 2-year-old toddlers. Subjects were drawn from a community sample, as part of a larger study of mothers and their children. Participants consisted of 99 toddlers and their mothers taken from a community sample. Fifty-two of the mothers smoked throughout pregnancy, while 47 either stopped smoking during pregnancy or started smoking after childbirth. Measures included assessment of smoking behavior, the mother's personality/behavior, perinatal variables, demographic variables, and aspects of the mother-child relationship. Using logistic regression analyses, maternal smoking during pregnancy was found to be related to negativity in the child, controlling for demographic factors, perinatal factors, maternal personality attributes, and the mother-child relationship. Findings suggest that maternal smoking during pregnancy has an adverse effect on the child's negativity, and that a decrease in maternal smoking during pregnancy might be expected to lead to a decrease in the child's negativity. The relationship of maternal smoking during pregnancy and early childhood negativity to other problem behaviors remains to be explored. Brook, J.S., Brook, D.W., and Whiteman, M. The Influence of Maternal Smoking During Pregnancy on the Toddler's Negativity. Arch Pediatr Adolesc Med, 154(4), pp. 381-385, 2000.


About NIDA Contents