Tritiated-naloxone binding to brainstem opioid receptors in the sudden infant death syndrome

Abstract

The sudden infant death syndrome (SIDS) is defined as the sudden death of an infant under 1 year of age that remains unexplained after a thorough case investigation, including a complete autopsy. We hypothesized that SIDS is associated with altered 3 H−naloxone binding to opioid receptors in brainstem nuclei related to respiratory and autonomic control. We analyzed 3 H−naloxone binding in 21 regions in SIDS and control brainstems using quantitative tissue receptor autoradiography. Three groups were analyzed: SIDS ( n=45); acute controls ( n=14); and a chronic group with oxygenation disorders ( n=15). Opioid binding was heavily concentrated in the caudal nucleus of the solitary tract, nucleus parabrachialis medialis, spinal trigeminal nucleus, inferior olive, and interpeduncular nucleus in all cases analyzed ( n=74). The arcuate nucleus on the ventral medullary surface contained negligible binding in all cases ( n=74), and therefore binding was not measurable at this site. We found no significant differences among the three groups in the age-adjusted mean 3 H−naloxone binding in 21 brainstem sites analyzed. The only differences we have found to date between SIDS and acute controls are decreases in 3 H−quinuclidinyl benzilate binding to muscarinic cholinergic receptors and in 3 H−kainate binding to kainate receptors in the arcuate nucleus in alternate sections of this same data set. The present study suggests that there is not a defect in opioid receptor binding in cardiorespiratory nuclei in SIDS brainstems.