SIDS is the inexplicable death of an infant, generally in their sleep, before their first birthday despite a thorough investigation for its cause.
Previous research in rodents has shown 2A/C receptor signalling to contribute to arousal and autoresuscitation, protecting brain oxygen status during sleep.
In this study, the researchers, including those from Boston Children’s Hospital, Massachusetts, US, examined the brain stems of 70 infants, who died between 2004 and 2011, and tested them for consistent abnormalities.
They found that the serotonin 2A/C receptor was altered in sudden infant death cases compared to control cases of infant deaths.
They have published their findings in the Journal of Neuropathology & Experimental Neurology.
The investigators believe that sudden infant death syndrome occurs when three things happen together: a child is in a critical period of cardiorespiratory development in their first year, the child faces an outside stressor like a face-down sleep position or sharing a bed, and the child has a biological abnormality that makes them vulnerable to respiratory challenges while sleeping.
“The work presented builds upon previous work by our laboratory and others showing abnormalities in the serotonergic system of some SIDS infants.
“Although we have identified abnormalities in the serotonin 2A/C receptor in SIDS, the relationship between the abnormalities and cause of death remains unknown.
“Much work remains in determining the consequence of abnormalities in this receptor in the context of a larger network of serotonin and non-serotonin receptors that protect vital functions in cardiac and respiratory control when challenged.
“Currently, we have no means to identify infants with biological abnormalities in the serotonergic system. Thus, adherence to safe-sleep practices remains critical,” said the paper’s lead author, Robin Haynes.