Loss of brainstem serotonergic neurons impairs autoresuscitation in neonate rats: is this relevant to the sudden infant death syndrome?

摘要

Sudden infant death syndrome, SIDS, remains the major cause of death among children less than a year old despite the identification of remediable environmental risk factors (air pollutants, nicotine, prone sleeping position, etc.). A plausible neuro-centric hypothesis posits that these risk factors matter only in the context of some pre-existing brainstem neurological deficit (Becker, 1990). Specifically, cardio-respiratory collapse and death would result from defective brainstem mechanisms that have evolved to protect against stressors that occur while asleep during a critical period of development. The crux of the matter may be the phenomenon called autoresuscitation and the key to autoresuscitation is gasping, an intense but short-lived activation of breathing that restores blood gases in extremis. Gasping is presumably caused by the direct activation of the preBotzinger complex by hypoxia (Paton et al. 2006).