"A normal baby will wake up, turn its head, and start breathing faster when carbon dioxide levels rise," explains Kinney.
But in babies who die from SIDS, defects in the serotonin system may impair these reflexes, the researchers believe.
Kinney previously documented serotonin receptor abnormalities in two other populations of SIDS infants, including American Indian infants in the Northern Plains, whose SIDS rate is among the highest in the world. The current study confirms those findings in a third population and, for the first time, pinpoints multiple defects in the serotonin system other than those in serotonin receptors: deficiencies in a particular type of serotonin receptor (called 5HT1A), an abnormally high number of serotonergic neurons (neurons that make and release serotonin), a preponderance of immature serotonergic neurons, and evidence for insufficient amounts of the serotonin transporter protein, which "recycles" serotonin so that nerve cells can reuse it.
"We provide strong evidence that SIDS is a biological problem, and that the brainstem serotonin system is a good place to focus continued research efforts," says Paterson.
He and Kinney believe that the abnormalities they observed begin during early fetal development, and that prenatal insults like maternal smoking and alcohol use may adversely affect development of the brainstem serotonin system during this time. More research is needed to explain what causes the abnormalities and how they can be prevented.
The findings also provide a biological explanation for why SIDS occurs twice as often in males than females ?male SIDS infants had significantly fewer 5-HT1A receptors than female SIDS infants.
In addition, serotonin abnormalities help explain why infants under 6 months are most vulnerable to SIDS.
Source:Children's Hospital Boston