New Clues to Sudden Infant Death Syndrome
Science may be a step closer to solving one of its most puzzling and heartbreaking mysteries -- the cause (and prevention) of sudden infant death syndrome (SIDS).
Researchers from the Geisel School of Medicine at Dartmouth, NH, recently investigated the role of serotonin on breathing responses in sleeping infants. The findings, published in Experimental Physiology, offer an exciting new avenue of research.
Guidelines to minimize the risk of SIDS (baby sleeping positions, avoiding soft surfaces, etc.) have resulted in significant decline in SIDS since 1990, from 130.3 deaths per 100,000 to 38.7 in 2014. But the goal is to reduce these numbers even further.
Previous findings demonstrated that the brainstems of infants who died of SIDS were deficient in both serotonin and serotonin receptors. This study investigated whether serotonin could shorten apnea (temporary breaks in breathing) and whether blocking serotonin would lengthen apnea.
The research was carried out in an animal model, using rat pups. When serotonin was injected into the brainstem, the apnea reduced in duration from around 10 seconds to 2 seconds. This effect was only measured when a specific type of serotonin receptor was activated -- the 5HT3 receptor.
This is a very encouraging step toward reducing or eliminating the syndrome. The team plans to continue this line of research to understand whether babies who die of SIDS are deficient in 5HT3 receptors. Other brain regions that might be involved in the laryngeal chemoreflex will also be explored.