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Identification of neurons responding to hypoxia in sudden infant death syndrome
Author(s) -
Lavezzi Anna Maria,
Ottaviani Giulia,
Matturri Luigi
Publication year - 2003
Publication title -
pathology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.73
H-Index - 74
eISSN - 1440-1827
pISSN - 1320-5463
DOI - 10.1046/j.1440-1827.2003.01556.x
Subject(s) - sudden infant death syndrome , medulla oblongata , dorsal motor nucleus , hypoxia (environmental) , nucleus , neuroscience , medulla , biology , control of respiration , immunohistochemistry , respiratory system , respiratory center , medicine , vagus nerve , pathology , anatomy , central nervous system , chemistry , stimulation , oxygen , pediatrics , organic chemistry
The pathogenesis of sudden infant death syndrome (SIDS) is still not understood, although one of the most credited current hypotheses is the respiratory theory. Considerable evidence has been assembled suggesting that hypoxia in human infants produces an initial increase in ventilation, after which respiration is rapidly inhibited. We investigated the expression of the c‐fos proto‐oncogene, a marker of activated neurons, particularly by hypoxia, in the medulla oblongata nuclei involved in breathing after birth, with special reference to SIDS. We utilized c‐fos protein immunohistochemistry on serial transverse sections of medulla oblongata from 22 SIDS victims. In 60% of the analyzed cases, we observed numerous positive c‐fos neurons in the dorsal motor nucleus of the vagal nerve. In control cases, the immunohistochemical labeling was negative or very low. The c‐fos protein was expressed in the rostral–intermediate portion of the dorsal motor vagal nucleus, where motoneurons with respiratory‐related activity are located. The positive c‐fos immunoreactivity observed in SIDS suggests that the neurons of the dorsal motor vagal nucleus involved in the regulation of breathing are able to yield an intense, immediate ventilatory response to hypoxia. Our results support the respiratory theory of SIDS.