Zili Luo, MD, Ph.D., a postdoctoral fellow in the laboratory of Dr. Ralph Fregosi, describes the study at the Experimental Biology 2003 meeting in San Diego, as part of the American Physiological Society program.
In humans, cases of Sudden Infant Death Syndrome (SIDS) occur most often in infants between the ages of two and four months, while the baby is sleeping. SIDS deaths usually are attributed to apnea or the cessation of breathing and the failure of the infant to self-resuscitate or resume breathing. Smoking during pregnancy has been found to increase the risk of Sudden Infant Death Syndrome (SIDS) by about five fold, and researchers have long been eager to pinpoint the mechanism by which this occurs.
Earlier studies by other investigators showed that prenatal nicotine exposure enhances the function and density of GABAa receptors in the cortex, hippocampus and other areas of the brain. These observations led the Fregosi laboratory to hypothesize that prenatal nicotine exposure may also alter the function or density of the GABAa receptors on cells in the brain regions that control breathing. In earlier work, the Fregosi laboratory had already sown that pharmacological stimulation of these inhibitory nerve cell membrane receptors led to slowing of the breathing rate, with intense stimulation leading to cessation of breathing altogether.
This study looked at whether prenatal nicotine enhances the function of these receptors, thus making it more likely that newborns that had been exposed to nicotine would have more episodes of apnea when the GABAa receptors are stim
Contact: Sarah Goodwin
Federation of American Societies for Experimental Biology