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

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 formati...

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Bibliographic Details
Published in:Experimental brain research 2014-08, Vol.232 (8), p.2455-2469
Main Authors: Yates, Bill J., Catanzaro, Michael F., Miller, Daniel J., McCall, Andrew A.
Format: Article
Language:English
Subjects:
Afferent Pathways - physiopathology
Analysis
Animals
Biological and medical sciences
Biomedical and Life Sciences
Biomedicine
Brain stem
Brain Stem - physiopathology
Diaphragm - physiopathology
Ear, auditive nerve, cochleovestibular tract, facial nerve: diseases, semeiology
Emetics - toxicity
Ent, stomatology, face, injuries. Foreign bodies. Diseases due to physical agents: otorhinolaryngology
Gastrointestinal Tract - drug effects
Humans
Medical sciences
Motion sickness
Motion Sickness - etiology
Muscle contraction
Nausea
Nausea - complications
Nausea - etiology
Neurology
Neurosciences
Non tumoral diseases
Otorhinolaryngology. Stomatology
Physiological aspects
Respiration
Review
Traumas. Diseases due to physical agents
Vestibule, Labyrinth - physiology
Vomiting
Vomiting - complications
Vomiting - etiology
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Summary: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 brain stem that result in emesis.
ISSN:0014-4819
1432-1106
DOI:10.1007/s00221-014-3937-6