Brainstem projections of sensory and motor components of the vagus nerve in the rat

Abstract

The sensory and motor connections of the cervical vagus nerves and of its inferior ganglion (nodose ganglion) have been traced in the medulla and upper cervical spinal cord of 16 male Wistar rats by using horseradish peroxidase (HRP) neurohistochemistry. The use of tetramethyl benzidine (TMB) as the substrate for HRP permitted the visualization of transganglionic and retrograde transport in sensory nerve terminals and perikarya, respectively. The vagus nerve in the rat enters the medulla in numerous fascicles with points of entry covering the entire lateral aspect of the medulla extending from level +4 to -6 mm rostrocaudal to the obex. Fascicles of vagal sensory fibers enter the dorsolateral aspect of the medulla and travel to the tractus solitarius (TS) which was labeled for over 8.8 mm in the medulla. The caudal extent of the TS receiving vagal projections was found in lamina V of the cervical spinal cord (C1 to C2). Sensory terminal fields could be visualized bilaterally in the nucleus of the tractus solitarius (nTS), area postrema (ap) and dorsal motor nucleus of the vagus nerve (dmnX). The ipsilateral projection to the nTS and the dmnX was heavier than that found on the contralateral side. The area postrema was intensely labeled on both sides. Motor fibers from HRP-labeled perikarya in the dmnX travel ventromedially in a distinct fascicle and subsequently subdivide into a number of small fiber bundles that traverse the medullary reticular formation in the form of a fine network of HRP-labeled fibers. As these fibers from the dmnX approach the ventrolateral aspect of the medulla they are joined by axons from the nucleus ambiguus (nA), nucleus retroambigualis (nRA) and the retrofacial nucleus (nRF). These latter fibers form hairpin loops in the middle of the reticular formation to accompany the axons from the dmnX exiting from the medulla in a ventrolateral location. HRP-labeled perikarya, in contrast to transganglionically transported HRP in sensory terminals in the nTS, were visualized on one side only, thus indicating that motor control via the vagus nerve is exerted only by motor neurons located ipsilaterally. Sensory information on the other hand, diverges to many nuclear subgroups located on both sides of the medulla.

GABA signaling in the nucleus tractus solitarius sets the level of activity in dorsal motor nucleus of the vagus cholinergic neurons in the vagovagal circuit

“…However, we do not feel that this is the case because contralateral vagal afferents also terminate in the area of the mNTS (14,20).…”

Excitatory and inhibitory local circuit input to the rat dorsal motor nucleus of the vagus originating from the nucleus tractus solitarius

“…The implications of this may be important for understanding how putative vagovagal reflexes are organized within the DVC. Afferents from the stomach tend to localize to the dorsomedial NTS, whereas baroreceptor input is concentrated in the medial NTS, respiratory sensation in the ventrolateral NTS, and pharyngeal sensation in the intermediate NTS [1,14]. Dendrites from any area might impinge on another area, so focal glutamate release-either from vagal afferent terminals or after glutamate photoactivation-might activate cells residing in another anatomical subdivision of the nucleus.…”

Increase in 20–50Hz (gamma frequencies) power spectrum and synchronization after chronic vagal nerve stimulation

“…Though VNS failed to show acute modifications following on and off periods of activation (Salinski and Burchiel, 1993), experimental evidences have suggested that electrical stimulation induced modification of brain rhythms via the nucleus tractus solitarius (NTS), which is the main site of visceral afferent complex termination and is regulated by cholinergic inputs (Beckstead and Norgren, 1979;Kalia and Sullivan, 1982;Rutecki, 1990;Schacther and Saper, 1998). However, the extended network of NTS connections (Saper, 1995) might mediate the biochemical and electrical effects of VNS through several mechanisms.…”

“…The mechanism of the therapeutic action of VNS remains unclear, however. Although its efficacy has been suggested to result from complex interactions of biochemical and electrical events (Beckstead and Norgren, 1979;Kalia and Sullivan, 1982;Rutecki, 1990), few studies have examined the effects of VNS on the EEG. …”