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 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.