IL NUCLEO RETROTRAPEZOIDE UMANO: ALTERAZIONI CONGENITE IN CASI DI MORTE INASPETTATA PERINATALE E DEL LATTANTE

Efficient uptake of oxygen and removal of carbon dioxide are essential conditions for life, and for normal growth and development in many species. Neurons in the brainstem chemoreceptors are distributed in specialized cental detect and regulate the presence of CO2 and/or changes in pH through a variety of responses. In so doing, these central chemoreceptors regulate extrauterin breathing actively responding through a variety of responses. Differences between prenatal and postnatal chemoreception appear to be primarily dependent on central inhibition in fetal life of the ventilatory responses to hypoxia and/or hypercapnia, with localization to the rostral lateral pons in the parabrachial/Kölliker-Fuse complex. The inhibitory effects of this complex are significantly reduced after the birth. Thus, chemoreception would function differently in the fetus than in the newborn, and birth would be associated with an abrupt change in the parabrachial/Kölliker-Fuse complex function. Experimental studies on animal models have identified the retrotrapezoide nucleus (RTN) as one of the main sites of central chemoreception and respiratory control. Numerous studies have RTN elected as one of the most important regions mediating central chemoreception. The RTN appears to integrate central and peripheral chemoreceptor information, providing an important role in respiratory function. The objectives of the study were: to locate and describe the cytoarchitecture of the nucleus retrotrapezoide (RTN) in the human fetus and infant, and ensure that the RTN, given its essential role in animal studies for the maintenance of respiration, showed abnormalities in victims of death sudden unexplained intrauterine (SIUD) and sudden infant syndrome (SIDS). Many studies have shown the expression of a transcription factor in neurons of the NRT: PHOX2B gene that was used as a marker. Three groups of Italians Caucasian children were autopsied, and by using immunohistochemistry has been studied the expression of PHOX2B gene. A group of positive neurons has been identified located within the caudal pons, contiguous to the facial/parafacial (PFN) complex, potentially the human homologous RTN (hRTN), already known in the mouse. In 71% of the cases has been observed structural abnormalities and/or expression of the PHOX2B gene hRTN vs. 10% of controls. In 85% of cases with alterations was also observed agenesis of the complex PFN. This study was conducted to determine the possibility of tracing the anatomical borders and cytoarchitecture of the human homologue of the RTN, by using immunohistochemical techniques. Views longstanding literature regarding the involvement of cardio-respiratory alterations in the sudden infant death syndrome (SIDS) pathogenesis, and the role of hNRT in regulation of breathing chemoreception, it has been hypothesized that abnormalities of development the RTN can play a critical role in SIDS and SIUD etiology.