Babies affected by sudden death would present an alteration of a serotonin receptor.
- Researchers examined the brainstems of 70 infants affected by sudden death.
- In the babies who died, the serotonin 5-HT2A/C receptor, which plays a role in regulating sleep and breathing, was impaired.
- When three factors come together, Sudden Infant Death Syndrome could occur.
In the United States, Sudden Infant Death Syndrome is the leading cause of post-neonatal infant death. This case where the death of a healthy baby occurs during sleep before his first birthday remains unexplained. For several years, researchers have been trying to discover the causes of this syndrome, which can strike any child without any prior sign of illness. Environmental factors, such as the position of the baby when sleeping, were examined.
Sudden infant death syndrome: the 5-HT2A/C serotonin receptor is altered
Recently, scientists from the University of Oxford (England) discovered that the problem could lie in the anatomy of the brain. To carry out their study, published in the journal Journal of Neuropathology & Experimental Neurologythey collected tissue from the San Diego Medical Examiner’s Office in connection with infant deaths that occurred between 2004 and 2011. The team analyzed the brainstems of 70 babies who died during this period and subjected them to testing to detect consistent anomalies.
She discovered abnormalities in the serotonin 5-HT2A/C receptor. The latter is a neurotransmitter present in the brain. According to previous research, in mice, 5-HT2A/C receptor signaling contributes to wakefulness and self-resuscitation, by protecting the oxygenation status of the brain during sleep.
Three factors together would trigger sudden infant death syndrome
According to the authors, sudden infant death syndrome occurs when three factors come together: “the child is in a critical period of cardiorespiratory development during the first year, is faced with an external stressor, such as a face-down sleeping position or shared bed, and exhibits a biological anomaly that makes him vulnerable to breathing problems while he sleeps.”
“Although we have identified abnormalities of the serotonin 5-HT2A/C receptor in Sudden Infant Death Syndrome, the link between these abnormalities and the cause of death remains unknown. Much remains to be done to determine the consequences of abnormalities of this receptor in the context of a larger network of serotonergic and non-serotonergic receptors that protect vital functions of cardiac and respiratory control when challenged.At present, we have no way to identify infants with biological abnormalities of the serotonergic system, so it is essential to follow safe sleep practices.”concluded Robin Haynes, author of the work, in a statement.