The leading cause of infant death in developed countries, sudden infant death syndrome, is still largely a medical mystery. Past studies have revealed that in the brain stems of more than half of infants who die from SIDS, the neurons that produce serotonin—a chemical responsible for regulating heart rate, body temperature and mood—are overly prevalent and abnormally shaped. Until now, no one has known how these problems might cause death, but a July 4 Science study reveals clues about what might be going wrong in SIDS and how doctors might prevent it.
Mood researchers at the European Molecular Biology Laboratory in Monterotondo, Italy, were investigating how serotonin levels affected anxiety-related behavior in mice when they got a surprise. They bred the mice to have too many 5-HT1A receptors, which are known to signal neurons to slow down the release of serotonin when the chemical is abundant in the brain. Having more receptors ultimately lowers serotonin levels and overall serotonin activity.
The team was startled to find that nearly three quarters of the mice died before they turned four months old, typically after suffering sudden drops in heart rate and body temperature so drastic that the complications killed the animals. Although the researchers do not yet know what prompts these crises, co-author Cornelius Gross speculates that they occur when serotonin activity cannot ramp up properly. For instance, serotonin systems are turned off during rapid-eye-movement (REM) sleep, so waking is typically accompanied by a rapid increase in serotonin activity. In the mice, Gross explains, the compromised 5-HT1A feedback loop may prevent serotonin neurons from firing when they should, disrupting nervous system function.
If Gross is right, the unexpected findings reveal how a seemingly simple alteration in the serotonin system can lead to infant death. Although SIDS babies have normal 5-HT1A receptors, one of their many other serotonin feedback mechanisms may be malfunctioning in a similar way. If so, the key to preventing SIDS could one day be as simple as finding a way to regulate abnormal serotonin feedback.
Note: This article was originally printed with the title, "Serotonin and SIDS".
