Sudden infant death syndrome is the primary cause of mortality in children aged one to six months in industrialized countries. Although the etiology of this syndrome is still unknown, subtle abnormalities in the neuronal circuitry involved in the control of respiratory activity are suspected. Since stereotaxic administration of somatostatin in the brainstem of rat and cat produces fatal apnea, we have compared the densities of somatostatin binding sites in the respiratory centers of 11 cases of sudden infant death syndrome and six control infants without neuronal disease. The density of binding sites was measured in 17 structures of the pons and medulla oblongata by means of quantitative in vitro autoradiography using iodinated [Tyr0,D-Trp8]somatostatin-14 as a radioligand. The density of somatostatin binding sites was significantly higher in the medial and lateral parabrachial nuclei in the sudden infant death syndrome group than in the control group. In six other nuclei, the median of the receptor density was higher in the sudden infant death syndrome group than the maximum values measured in the control group. The presence of high concentrations of somatostatin binding sites in several respiratory nuclei of the brainstem in approximately half of the sudden infant death syndrome victims suggests that the decrease in receptor density that normally occurs during ontogeny was delayed in these infants. In particular, the high level of somatostatin binding sites in the medial and lateral parabrachial nuclei of sudden infant death syndrome suggests that the delayed maturation of these receptors may be associated with a deficit of the hyperventilatory response to hypoxia.