Projections from the nucleus tractus solitarii to the spinal cord

Abstract

Projections from the nucleus tractus solitarii (NTS) to the spinal cord were demonstrated in the male Sprague-Dawley rat. In retrograde transport studies, a horseradish peroxidase conjugate or a fluorescent dye, FluoroGold, were injected into midcervical or upper thoracic spinal segments. Most solitariospinal neurons were multipolar or bipolar and located between the obex and spinomedullary junction. Solitariospinal neurons were concentrated in proximity to the ventral border of the solitary tract and extended dorsally into the intermediate division and ventrolaterally into the intermediate reticular zone (IRt) of the lateral tegmental field. This subgroup predominantly projects to midcervical spinal segments. A subset of small neurons was retrogradely labeled from cervical or thoracic spinal segments in the medial commissural nucleus and contiguous with a periventricular group surrounding the central canal. In anterograde transport studies, iontophoretic deposits of Phaseolus vulgaris leucoagglutinin were centered stereotaxically on sites in NTS identified by retrograde transport data. The lectin was incorporated by neurons of the solitary complex and transported bilaterally by axons that emerged from the nucleus and entered the reticular formation. The solitario-reticular (transtegmental) pathway irradiated diagonally across the IRt and extended caudally into the cervical lateral funiculus and spinal gray. A small periventricular-spinal pathway also descended longitudinally to the neuraxis. Solitariospinal neurons project to superficial lamina of the dorsal horn, laminae VII and X and ventral horn. The projections are predominantly contralateral to phrenic and intercostal motor nuclei and ipsilateral to the intermediolateral cell column. The solitariospinal projection represents the shortest route in the central nervous system, other than the local intraspinal reflex, through which first order visceral afferents signal cardiorespiratory and alimentary motor nuclei.

CCK enhances response to gastric distension by acting on capsaicin-insensitive vagal afferents

“…Signals from spinal afferents probably reach the NTS via the spinosolitary tract (19,22,43). It might be that high-volume distension activates these spinal pathways as well as activating vagal afferents.…”

Left vagal stimulation induces dynorphin release and suppresses substance P release from the rat thoracic spinal cord during cardiac ischemia

“…Both are reported to reduce intractable angina with no adverse cardiovascular consequences (18,28,32,42,43,54,55). Widespread clinical studies are limited, and how such approaches exert their antianginal effects is not well defined, but the mechanisms likely involve both cardiac (18,28,54,55) and neuromodulator (18,28,34,38,55) components. While the electrical stimulation vs. coronary bypass study indicates that neuromodulation therapy is an effective treatment option for patients with chronic refractory angina (15), further and more extensive clinical investigation would be needed to verify the efficacy of these techniques as an antianginal therapy.…”

“…Neurons in this pathway, in turn, are activated by vagal stimulation. Alternately, because it is well documented that vagal afferent information synapses directly into the NTS, some of the inhibitory effects of vagal stimulation may be due to activation of descending pathways from the NTS to the cervical spinal cord (16,38). The NTS has a high concentration of SP immunoreactivity (48), and projections from NTS sites via relays, either through the pons or rostroventrolateral medulla (42,43), may transmit an inhibitory signal to the spinal cord.…”

Inhibition of brown adipose tissue thermogenesis by neurons in the ventrolateral medulla and in the nucleus tractus solitarius

“…As discussed above for the BAT sympathoinhibitory neurons in the VLM, the spinal cord is a potential site at which NTS neurons could act to inhibit BAT SNA, since NTS neurons project to the medial and intermediolateral regions of the thoracic spinal cord (2,28,38). Since the effect on BAT SNA of activating intermediate NTS neurons was not tested following pontomedullary transection, no conclusions can be drawn regarding the role of supramedullary pathways in the BAT inhibition evoked from the intermediate NTS.…”