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A University of Chicago professor explains his findings that serotonin induces gasping in oxygen-deprived infants. These results will probably not lead to Prozac prescriptions for babies, but they could be used to find a genetic marker for SIDS risk down the road.
Sudden Infant Death Syndrome could be caused by a problem with serotonin receptors on a specific type of neuron, according to a paper published in the March 8 Journal of Neuroscience.
The study provides a mechanism that could explain why infants are more likely to experience SIDS when sleeping on their stomachs, and it raises the possibility that infants at risk could ultimately be identified by a genetic test.
The study focuses on a group of neurons called CI-pacemakers, which the study’s authors believe are responsible for gasping. The neurons have serotonin receptors on their surfaces, and when serotonin binds to the receptors it opens channels that allow a burst of calcium to flow into the neuron. This burst causes the pacemaker neurons to induce gasping.
According to lead author Jan-Marino Ramirez, an assistant professor of organismal biology at the University of Chicago, babies who die of SIDS have an insufficient ability to gasp. When a sleeping infant is deprived of oxygen, for example because of lying on its stomach, the CI-pacemakers would normally cause the infant to gasp, and gasping would cause the baby to wake up crying, which would reset normal breathing. At this point, it might also turn over on its own or be aided by a concerned parent.
Previous studies have shown that infants who died of SIDS had abnormal serotonin transporters, the receptor that takes serotonin into cells for recycling, Ramirez explained. The serotonin transporter is different from the serotonin receptor found on the pacemaker neurons. But because it is involved in moving serotonin into cells, it plays a role in regulating the amount of serotonin present in the body.
At this point, it is unclear how the disturbed serotonin transporters are linked to the pacemaker neurons that control gasping, Ramirez said. The problem with the transporters could lead to decreased levels of serotonin in the body, he said. On the other hand, he theorized, it could lead to increased levels, which, in turn, could make the body downgrade production of serotonin.
Further research should develop the link between the pacemaker neurons and the disturbed serotonin transporters, according to Ramirez. He is also interested in learning about the connection between pacemaker neurons and the brain’s center for arousal, the locus coeruleus.
In the clinic, it may be possible to identify babies at a high risk for SIDS by screening for disturbances in serotonin levels or serotonin transporters, Ramirez said. Looking down the road, it might be possible to identify a genetic marker that would allow physicians to associate the baby’s risk with a number.
It is possible that if a marker were found, babies at high risk for SIDS could be given a drug to normalize their serotonin levels, he said. But for now, Ramirez is very reluctant to use drugs that increase levels of serotonin, such as antidepressants, to correct this problem. Serotonin is a complicated molecule, which affects many systems, he explained. At this stage of understanding, it would be better to just monitor babies who are at high risk very carefully.