The brainstem and serotonin in the sudden infant death syndrome.
The sudden infant death syndrome (SIDS) is the sudden death of an infant under one year of age that is typically associated with sleep and that remains unexplained after a complete autopsy and death scene investigation. A leading hypothesis about its pathogenesis is that many cases result from defects in brainstem-mediated protective responses to homeostatic stressors occurring during sleep in a critical developmental period. Here we review the evidence for the brainstem hypothesis in SIDS with a focus upon abnormalities related to the neurotransmitter serotonin in the medulla oblongata, as these are the most robust pathologic findings to date. In this context, we synthesize the human autopsy data with genetic, whole-animal, and cellular data concerning the function and development of the medullary serotonergic system. These emerging data suggest an important underlying mechanism in SIDS that may help lead to identification of infants at risk and specific interventions to prevent death.
Kinney
Hannah C
HC
Department of Pathology, Children's Hospital Boston and Harvard Medical School, Boston, MA 02115, USA. Hannah.Kinney@childrens.harvard.edu
Richerson
George B
GB
Dymecki
Susan M
SM
Darnall
Robert A
RA
Nattie
Eugene E
EE
D000818:Animals; D001933:Brain Stem / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D007223:Infant; D009474:Neurons / Q000378:metabolism* / Q000473:pathology; D018570:Risk Assessment; D012307:Risk Factors; D012701:Serotonin / Q000378:metabolism*; D013398:Sudden Infant Death / Q000209:etiology* / Q000473:pathology / Q000517:prevention & control
D012701:Serotonin