The central connections of the vagus nerve in the ferret

Knox, A.P.; Strominger, Norman L.; Battles, August H.; Carpenter, David O.

doi:10.1016/0361-9230(94)90048-5

Cited by 16 publications

(3 citation statements)

References 108 publications

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“…Injection of emetic drugs such as apomorphine (Miller and Ruggiero 1994), whose action occurs centrally at area postrema (Borison 1959; Borison et al 1975), additionally induced Fos expression in NTS. Since NTS receives a large fraction of the efferent projections from area postrema (Leslie and Gwyn 1984; Knox et al 1994; Miller and Leslie 1994), this observation is also not unexpected. Fos expression also increases in NTS of shrews during emesis provoked by shaking, which presumably is associated with motion sickness (Ito et al 2003; Ito et al 2005).…”

Section: Brainstem Regions That Participate In Producing Nausea and Vmentioning

confidence: 77%

Integration of vestibular and emetic gastrointestinal signals that produce nausea and vomiting: potential contributions to motion sickness

et al. 2014

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Vomiting and nausea can be elicited by a variety of stimuli, although there is considerable evidence that the same brainstem areas mediate these responses despite the triggering mechanism. A variety of experimental approaches showed that nucleus tractus solitarius, the dorsolateral reticular formation of the caudal medulla (lateral tegmental field), and the parabrachial nucleus play key roles in integrating signals that trigger nausea and vomiting. These brainstem areas presumably coordinate the contractions of the diaphragm and abdominal muscles that result in vomiting. However, it is unclear whether these regions also mediate the autonomic responses that precede and accompany vomiting, including alterations in gastrointestinal activity, sweating, and changes in blood flow to the skin. Recent studies showed that delivery of an emetic compound to the gastrointestinal system affects the processing of vestibular inputs in the lateral tegmental field and parabrachial nucleus, potentially altering susceptibility for vestibular-elicited vomiting. Findings from these studies suggested that multiple emetic inputs converge on the same brainstem neurons, such that delivery of one emetic stimulus affects the processing of another emetic signal. Despite the advances in understanding the neurobiology of nausea and vomiting, much is left to be learned. Additional neurophysiologic studies, particularly those conducted in conscious animals, will be crucial to discern the integrative processes in the brainstem that result in emesis.

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Section: Brainstem Regions That Participate In Producing Nausea and Vmentioning

confidence: 77%

Integration of vestibular and emetic gastrointestinal signals that produce nausea and vomiting: potential contributions to motion sickness

et al. 2014

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“…The same study showed that a small number of DMX neurons penetrated the ependyma of the fourth ventricle (80). Moreover, the DMX has been shown to interact with the area postrema via both afferents (80,102,103) and efferents (80,104). The central nucleus of the amygdala in the rat sends a considerable projection to, and receives projections from, the parabrachial nucleus and the dorsal vagal complex (DVC; constituents of the DVC are the NST and the DMX) (105).…”

Section: Resultsmentioning

confidence: 99%

Vagus nerve stimulation for primary headache disorders: An anatomical review to explain a clinical phenomenon

et al. 2019

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Background Non-invasive stimulation of the vagus nerve has been proposed as a new neuromodulation therapy to treat primary headache disorders, as the vagus nerve is hypothesized to modulate the headache pain pathways in the brain. Vagus nerve stimulation can be performed by placing an electrode on the ear to stimulate the tragus nerve, which contains about 1% of the vagus fibers. Non-invasive vagus nerve stimulation (nVNS) conventionally refers to stimulation of the cervical branch of the vagus nerve, which is made up entirely of vagal nerve fibers. While used interchangeably, most of the research to date has been performed with nVNS or an implanted vagus nerve stimulation device. However, the exact mechanism of action of nVNS remains hypothetical and no clear overview of the effectiveness of nVNS in primary headache disorders is available. Methods In the present study, the clinical trials that investigated the effectiveness, tolerability and safety of nVNS in primary headache disorders were systematically reviewed. The second part of this study reviewed the central connections of the vagus nerve. Papers on the clinical use of nVNS and the anatomical investigations were included based on predefined criteria, evaluated, and results were reported in a narrative way. Results The first part of this review shows that nVNS in primary headache disorders is moderately effective, safe and well-tolerated. Regarding the anatomical review, it was reported that fibers from the vagus nerve intertwine with fibers from the trigeminal, facial, glossopharyngeal and hypoglossal nerves, mostly in the trigeminal spinal tract. Second, the four nuclei of the vagus nerve (nuclei of the solitary tract, nucleus ambiguus, spinal nucleus of the trigeminal nerve and dorsal motor nucleus (DMX)) show extensive interconnections. Third, the efferents from the vagal nuclei that receive sensory and visceral input (i.e. nuclei of the solitary tract and spinal nucleus of the trigeminal nerve) mainly course towards the main parts of the neural pain matrix directly or indirectly via other vagal nuclei. Conclusion The moderate effectiveness of nVNS in treating primary headache disorders can possibly be linked to the connections between the trigeminal and vagal systems as described in animals.

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“…The results obtained in experiment 1 may be explained, on the one hand, because the vagal visceral information is specifically interrupted. It must not be ignored that the PPN receives information from the STN and the parabrachial region (Semba & Fibiger, 1992;Steckler et al, 1994b), relay areas for vagal information processing (Cecheto, 1987;Gieroba & Blessing, 1994;Hermann & Roger, 1985;Knox, Strominger, Battles, & Carpenter, 1994;Kobashi, Ichikawa, Sugimoto, & Adachi, 1993).…”

Section: Discussionmentioning

confidence: 99%

Electrolytic Lesions of the Pedunculopontine Nucleus Disrupt Concurrent Learned Aversion Induced by NaCl

Mediavilla

Molina

Puerto

2000

Neurobiology of Learning and Memory

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Bilateral electrolytic lesions in the pedunculopontine nucleus (PPN) impair acquisition of short-term, or concurrent, Taste Aversion Learning (TAL) in rats. This type of TAL is characterized by the daily presentation of two different flavor stimuli at the same time, one associated with simultaneous intragastric administration of an aversive product (hypertonic NaCl) and the other with physiological saline. Sham-lesioned control animals learn this taste discrimination task, but both lesioned animals and control animals learn a long-term, or delayed, TAL task in which each gustatory stimulus is presented individually every other day and the intragastric products, LiCl (0.15 M) and physiological saline, are administered after a 15-min delay. These results are analyzed in the context of the cerebellar circuits involved in learning and in relation to the two TAL modalities described above. ᭧ 2000 Academic Press

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The central connections of the vagus nerve in the ferret

Cited by 16 publications

References 108 publications

Integration of vestibular and emetic gastrointestinal signals that produce nausea and vomiting: potential contributions to motion sickness

Integration of vestibular and emetic gastrointestinal signals that produce nausea and vomiting: potential contributions to motion sickness

Vagus nerve stimulation for primary headache disorders: An anatomical review to explain a clinical phenomenon

Electrolytic Lesions of the Pedunculopontine Nucleus Disrupt Concurrent Learned Aversion Induced by NaCl

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