Sudden infant death syndrome and serotonin: animal models

Abstract

The sudden infant death syndrome (SIDS) is the sudden, unexpected death of an infant that is not explained by autopsy, death scene examination, and history. The etiology is unknown. Recent postmortem studies have discovered abnormalities in brainstem serotonergic neurons, but how these translate into dysfunction and cause SIDS is uncertain. Recently, lethal effects in transgenic mice with overexpression of the serotonin 1A autoreceptor have been described. Many die spontaneously between postnatal day 40 (P40) and P80, and some spontaneously exhibit bradycardias and drops in body temperature. The severity of the autonomic dysfunction and its age dependence suggest relevance to SIDS. However, SIDS cases have decreased serotonin 1A autoreceptor binding, which is opposite to its overexpression in the mice, and the peak incidence of SIDS is between 2 and 6 months of age, which is arguably younger (in relative terms) than the ages at which the mice die. Nevertheless, the description of an animal model with serotonin defects that has autonomic dysfunction and spontaneous mortality at a young age is an exciting finding of possible importance for understanding SIDS.