New evidence of serotonergic dysfunction in sudden infant death syndrome

Paterson DS et al. (2006) Multiple serotonergic brainstem abnormalities in sudden infant death syndrome. JAMA 296: 2124–2132

Sudden infant death syndrome (SIDS) is a major cause of postneonatal infant death, but despite considerable research into the condition the underlying biological mechanisms remain unclear. Abnormal binding patterns of the 5-hydroxytryptamine (5-HT; serotonin) receptors have previously been reported in cases of SIDS, and in a recent postmortem study of SIDS infants, researchers have found new evidence of cellular alterations within the serotonergic system of the medulla oblongata.

Paterson et al. obtained frozen medullae from 31 infants who had died from SIDS and from 10 infants who had died acutely from other causes (controls). The number and density of serotonergic neurons within the medullae were determined using immunocytochemistry, and the binding densities of the 5-HT_1A receptor and 5-HT transporter were assessed with autoradiography. The researchers also investigated potential correlations between their results and known risk factors for SIDS.

In SIDS cases, regions of the medulla involved in homeostatic function had significantly higher serotonergic neuron counts and densities than those of controls (P <0.001 for both), and significantly lower 5-HT_1A receptor binding densities (P ≤0.01). In the raphé obscurus, male SIDS cases had significantly lower 5-HT_1A receptor binding densities than female SIDS cases (P = 0.04).

The authors conclude that the medullary serotonergic abnormalities in SIDS cases are more extensive than have previously been reported, and that their results generate new hypotheses regarding 5-HT-related brainstem pathology in early sudden death. They also suggest that the lower levels of 5-HT_1A receptor binding density in male SIDS cases than in female cases might explain the particular vulnerability of males to this condition.