Serotonin is a neurotransmitter best known for its influence on depression and sexual function. But it also plays less famous roles: serotonin-releasing neurons in the brain stem regulate our body temperature and how we breathe. Henry Krous, a professor of pathology and pediatrics at the University of California, San Diego, and his colleagues have found that a failure of this system may be responsible for sudden infant death syndrome, or SIDS.
SIDS is diagnosed when a sleeping baby dies without obvious cause. An infant who is sleeping face down or who is too warm is more likely to die of SIDS. But this new research suggests some babies may be particularly at risk.
The researchers compared brain stem tissue from 31 infants who died from SIDS with samples from babies who died of trauma. In the SIDS brains the number of serotonin-responding neurons was much higher; however, protein receptors that detect serotonin and transporters responsible for clearing it from the synapses were both in short supply. These signs point to disruption of the system that monitors babies' oxygen intake and body temperature and should arouse them if, for example, a pillow makes it difficult for them to breathe. “In a way, it's comforting for parents,” Krous says; they are not to blame. “The defects are inherent to the baby.”
It would be ideal to screen for infants susceptible to SIDS at birth with, for example, a genetic test. But the researchers could not find a genetic defect in the infants that accounted for these brain stem abnormalities. Unfortunately, the method the team used to find neuronal defects is of no use clinically, as Elliott Sherr, a neurologist at the University of California, San Francisco, points out: “You're not going to do a brain biopsy on every baby.” But Sherr thinks that animal models of the brain stem defect could ultimately reveal ways to detect the serotonin-neuron defect in a blood sample.