Nausea and
vomiting are
biological systems for defense against
food poisoning that are also provoked by numerous drugs (e.g.,
chemotherapy,
anesthesia) and
chronic diseases (e.g.,
cancer, diabetic
gastroparesis). The sensory pathways that stimulate
nausea and
vomiting include vestibular, area postrema, and forebrain inputs, but gastrointestinal vagal afferent fibers arguably play the most prominent role as a first-line defense. Vagal sensory neurons detect toxins that enter the gastrointestinal lumen and transmit information to the hindbrain, leading to
nausea (an unconditioned stimulus that serves to facilitate the avoidance of offending foods) and
vomiting (a mechanism to clear contents from the stomach). Despite the major importance of these systems to human physiology, progress on the
biological basis of
nausea and
vomiting has been slow - partly because laboratory rats and mice, which represent the largest thrust of preclinical biomedical research, lack a
vomiting reflex (although they appear to have indices of
nausea, e.g., conditioned food aversion). Several established models are a mainstay of preclinical
nausea and
vomiting research in academia and
pharmaceutical companies, including the dog, cat, ferret, and
musk shrew. An argument is made for broader testing across species since each model possesses often unique experimental advantages and sensitivity to
emetic and
antiemetic agents. This review focuses on the state of knowledge on the neural pathways for
nausea and
vomiting, behavioral indices of
nausea used in preclinical models, role of vagal afferent fibers, current
antiemetic and antinausea treatments, and potential future directions.