Nausea and
vomiting are amongst the most common symptoms encountered in medicine as either symptoms of diseases or side effects of treatments. In a more
biological setting they are also important components of an organism's defences against ingested toxins. Identification of treatments for
nausea and
vomiting and reduction of
emetic liability of new
therapies has largely relied on the use of animal models, and although such models have proven invaluable in identification of the
anti-emetic effects of both 5-hydroxytryptamine(3) and
neurokinin(1) receptor antagonists selection of appropriate models is still a matter of debate. The present paper focuses on a number of controversial issues and gaps in our knowledge in the study of the physiology of
nausea and
vomiting including: The choice of species for the study of
emesis and the underlying behavioural (e.g. neophobia), anatomical (e.g. elongated, narrow abdominal oesophagus with reduced ability to shorten) and physiological (e.g. brainstem circuitry) mechanisms that explain the lack of a
vomiting reflex in certain species (e.g. rats); The choice of response to measure (
emesis[retching and
vomiting], conditioned flavour avoidance or aversion, ingestion of
clay[
pica], plasma
hormone levels[e.g.
vasopressin], gastric dysrhythmias) and the relationship of these responses to those observed in humans and especially to the sensation of
nausea; The stimulus coding of
nausea and
emesis by abdominal visceral afferents and especially the vagus-how do the afferents encode information for normal postprandial sensations,
nausea and finally
vomiting?; Understanding the central processing of signals for
nausea and
vomiting is particularly problematic in the light of observations that
vomiting is more readily amenable to pharmacological treatment than is
nausea, despite the assumption that
nausea represents "low" intensity activation of pathways that can evoke
vomiting when stimulated more intensely.