Abstract
Nausea and vomiting are common gastrointestinal complaints that can be triggered by diverse emetic stimuli through central and/or peripheral nervous systems. Both nausea and vomiting are considered as defense mechanisms when threatening toxins/drugs/bacteria/viruses/fungi enter the body either via the enteral (e.g., the gastrointestinal tract) or parenteral routes, including the blood, skin, and respiratory systems. While vomiting is the act of forceful removal of gastrointestinal contents, nausea is believed to be a subjective sensation that is more difficult to study in nonhuman species. In this review, the authors discuss the anatomical structures, neurotransmitters/mediators, and corresponding receptors, as well as intracellular emetic signaling pathways involved in the processes of nausea and vomiting in diverse animal models as well as humans. While blockade of emetic receptors in the prevention of vomiting is fairly well understood, the potential of new classes of antiemetics altering postreceptor signal transduction mechanisms is currently evolving, which is also reviewed. Finally, future directions within the field will be discussed in terms of important questions that remain to be resolved and advances in technology that may help provide potential answers.
Highlights
Nausea and vomiting are essential protective defense processes by which humans as well as vomit-competent animals tend to avoid ingestion and/or digestion of potentially toxic substances
The area postrema the sensory vagal afferents, afferents, the nucleusarea of the solitary tract is the recipient of: (i) Besides direct neural inputs from theand splanchnic nerves carrying the nucleus of the solitary tract is the recipient of: (i) direct neural inputs from the splanchnic nerves carrying sensation caused by diseases of visceral organs; (ii) brainstem vestibular nuclei collecting signals from vestibular apparatus in inner ear and/or cerebellum, caused by stimuli related to motion sickness and opioid analgesics [13,14]; and (iii) the cerebral cortex and limbic system, which accept and process emotional and cognitive stimuli [3–8]
The key sites in the mediation of vomiting are: (i) the brainstem dorsal vagal complex emetic nuclei such as the area postrema (AP), the nucleus of the solitary tract, and the dorsal motor nucleus of the vagus (DMNV) and (ii) the peripheral sites, including the sentinel epithelial enterochromaffin cells, which are present in the mucosa of gastrointestinal tract; the enteric nervous system embedded in the wall of gastrointestinal tract; and the vagus and splanchnic nerves
Summary
Nausea and vomiting are essential protective defense processes by which humans as well as vomit-competent animals tend to avoid ingestion and/or digestion of potentially toxic substances. Nausea and vomiting can be triggered by several mechanisms, as depicted, including: (i) toxins/drugs/bacteria/viruses/fungi that enter the lumen of the gastrointestinal and, subsequently, indirectly stimulate the brainstem emetic nuclei located in the dorsal vagal complex via release of local emetic neurotransmitters in the upper gastrointestinal tract and subsequent activation of corresponding receptors present on vagus nerves. The area postrema the sensory vagal afferents, afferents, the nucleusarea of the solitary tract is the recipient of: (i) Besides direct neural inputs from theand splanchnic nerves carrying the nucleus of the solitary tract is the recipient of: (i) direct neural inputs from the splanchnic nerves carrying sensation caused by diseases of visceral organs (e.g., cardiac, kidney); (ii) brainstem vestibular nuclei collecting signals from vestibular apparatus in inner ear and/or cerebellum, caused by stimuli related to motion sickness and opioid analgesics [13,14]; and (iii) the cerebral cortex and limbic system, which accept and process emotional and cognitive stimuli [3–8]. Understanding the circuitry and cellular mechanisms of nausea and vomiting helps us in developing new medications for the prevention and treatment of these debilitating symptoms
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