The 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.
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.
Duncan
Jhodie R
JR
Department of Pathology, Children's Hospital and Harvard Medical School, Boston, MA 02115, USA. jhodie.duncan@childrens.harvard.edu
Randall
Leslie L
LL
Belliveau
Richard A
RA
Trachtenberg
Felicia L
FL
Randall
Bradley
B
Habbe
Donald
D
Mandell
Federick
F
Welty
Thomas K
TK
Iyasu
Solomon
S
Kinney
Hannah C
HC
D000328:Adult; D000428:Alcohol Drinking / Q000009:adverse effects*; D020268:Alcohol-Induced Disorders, Nervous System / Q000208:ethnology / Q000378:metabolism / Q000473:pathology; D001667:Binding, Competitive / Q000187:drug effects / Q000502:physiology; D001933:Brain Stem / Q000378:metabolism* / Q000473:pathology; D002492:Central Nervous System Depressants / Q000009:adverse effects; D002799:Cholinergic Fibers / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D015331:Cohort Studies; D000431:Ethanol / Q000009:adverse effects; D005260:Female; D006801:Humans; D007198:Indians, North American / Q000208:ethnology; D007231:Infant, Newborn; D009538:Nicotine / Q000009:adverse effects; D018722:Nicotinic Agonists / Q000009:adverse effects; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000208:ethnology / Q000378:metabolism* / Q000473:pathology; D011869:Radioligand Assay; D011978:Receptors, Nicotinic / Q000187:drug effects / Q000378:metabolism*; D012125:Respiratory Center / Q000378:metabolism / Q000473:pathology; D012307:Risk Factors; D012907:Smoking / Q000009:adverse effects*; D013398:Sudden Infant Death / Q000208:ethnology / Q000473:pathology*
D002492:Central Nervous System Depressants; D018722:Nicotinic Agonists; D011978:Receptors, Nicotinic; D000431:Ethanol; D009538:Nicotine