Open AccessThe Effect of Maternal Smoking and Drinking During Pregnancy Upon 3 H‐Nicotine Receptor Brainstem Binding in Infants Dying of the Sudden Infant Death Syndrome: Initial Observations in a High Risk Population
Author(s) -
Duncan Jhodie R.,
Randall Leslie L.,
Belliveau Richard A.,
Trachtenberg Felicia L.,
Randall Bradley,
Habbe Donald,
Mandell Federick,
Welty Thomas K.,
Iyasu Solomon,
Kinney Hannah C
Publication year - 2008
Publication title -
brain pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.986
H-Index - 132
eISSN - 1750-3639
pISSN - 1015-6305
DOI - 10.1111/j.1750-3639.2007.00093.x
Subject(s) - sudden infant death syndrome , nicotine , brainstem , nicotinic agonist , pregnancy , medicine , cotinine , cholinergic , endocrinology , physiology , receptor , biology , pediatrics , genetics
The high rate of the sudden infant death syndrome (SIDS) in American Indians in the Northern Plains (3.5/1000) may reflect the high incidence of cigarette smoking and alcohol consumption during pregnancy. Nicotine, a neurotoxic component of cigarettes, and alcohol adversely affect nicotinic receptor binding and subsequent cholinergic development in animals. We measured 3 H‐nicotine receptor binding in 16 brainstem nuclei in American Indian SIDS (n = 27) and controls (n = 6). In five nuclei related to cardiorespiratory control, 3 H‐nicotinic binding decreased with increasing number of drinks ( P < 0.03). There were no differences in binding in SIDS compared with controls, except upon stratification of prenatal exposures. In three mesopontine nuclei critical for arousal there were reductions ( P < 0.04) in binding in controls exposed to cigarette smoke compared with controls without exposure; there was no difference between SIDS cases with or without exposure. This study suggests that maternal smoking and alcohol affects 3 H‐nicotinic binding in the infant brainstem irrespective of the cause of death. It also suggests that SIDS cases are unable to respond to maternal smoking with the “normal” reduction seen in controls. Future studies are needed to establish the role of adverse prenatal exposures in altered brainstem neurochemistry in SIDS.