Alpha2-adrenergic receptor subtype alterations in the brainstem in the sudden infant death syndrome

The sudden infant death syndrome (SIDS) is still the main cause of postneonatal infant death. However, the causes and mechanisms of SIDS have never been completely elucidated. Catecholamines, via alpha2-adrenergic receptor (alpha2-AR) interactions, are known to influence brainstem autonomic and respiratory activity.

To examine the catecholaminergic system abnormalities in SIDS victims, we investigated the alterations of alpha2-AR subtypes.

We examined the developmental changes of alpha2-AR subtypes in the brainstem, especially in cardiorespiratory nuclei, in 21 SIDS victims and 17 age-matched controls by means of immunohistochemical methods. For statistical analysis, the chi2-test or Fisher's exact probability test was performed.

There was a significant decrease in alpha2A-AR immunoreactivity in the solitary nucleus and ventrolateral medulla (VLM) in the medulla oblongata in SIDS victims compared with in control cases, but there were no significant differences of the alpha2B and alpha2C-AR immunoreactivity in the brainstem between SIDS victims and controls.

Alpha2A-AR immunoreactivity was selectively decreased in the solitary nucleus and VLM in the medulla oblongata in SIDS victims, so there was no possibility that it was secondary to chronic hypoxia or repeated ischemia. It may be related to some impairment of the cardiorespiratory neuronal system. Therefore, SIDS victims may be vulnerable to asphyxia, hypoxia, and/or hypercapnia, and fail to exhibit brainstem responses.