Anatomic relationships of the human nucleus of the solitary tract in the medulla oblongata: a DiI labeling study

The nucleus of the solitary tract (nTS) is a major site of brainstem control of vital functions (e.g., cardiovascular reflexes and respiration). We examined anatomic relationships of the human nucleus of the solitary tract, using a bidirectional lipophilic fluorescent tracer 1-1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate (DiI) in 10 postmortem human fetal midgestational medullae oblongatae. Labeling by diffusion of DiI from the nucleus of the solitary tract included: (1) neuropil of all future subdivisions of the nucleus of the solitary tract ipsilateral to the DiI crystal; (2) stellate cells in the caudal raphe at the junction of the nucleus raphe pallidus and the arcuate nucleus at the ventral medullary surface, as well as single fibers along the caudal raphe and the arcuate nucleus; (3) cells and fibers in other medullary areas related to autonomic and respiratory control, including the dorsal motor nucleus of the vagus, nucleus ambiguus complex/ventral respiratory group, rostral ventrolateral medulla (RVLM) and caudal ventrolateral medulla (CVLM), and medullary reticular formation. The pattern of connections of the nucleus of the solitary tract already established by midgestation in the human fetus is consistent with the pattern previously demonstrated in adult experimental animals. A major finding of the study is that of the stellate cells at the junction of nucleus raphe pallidus and the arcuate nucleus at the ventral medullary surface, which project to the nucleus of the solitary tract, and could be homologous to chemosensitive serotonergic neurons at the midline ventral medullary surface of experimental animals. This connection between the ventral caudal raphe and the nucleus of the solitary tract may participate in chemoreception and central regulation of cardiorespiratory reflexes during human perinatal development; it is, therefore, relevant to the study of sudden infant death syndrome (SIDS). (C) 2003 Elsevier Science B.V. All rights reserved.