The area postrema, a paired structure in the medulla oblongata of the brainstem,[1] is a circumventricular organ having permeable capillaries and sensory neurons that enable its dual role to detect circulating chemical messengers in the blood and transduce them into neural signals and networks.

Such roles of the area postrema include its detection of circulating hormones involved in vomiting, thirst, hunger, and blood pressure control.

It is excited by visceral afferent impulses (sympathetic and vagal) arising from the gastrointestinal tract and other peripheral trigger zones, and by humoral factors.

Nausea is most likely induced via stimulation of the area postrema via its connection to the NTS, which may serve as the beginning of the pathway triggering vomiting in response to various emetic inputs.

However, this structure plays no key role for nausea induced by the activation of vagal nerve fibers or by motion, and its function in radiation-induced vomiting remains unclear.

The area postrema is a critical homeostatic integration center for humoral and neural signals by means of its function as a chemoreceptor trigger zone for vomiting in response to emetic drugs.

[2][6] Angiotensin II causes a dose-dependent increase in arterial blood pressure without producing considerable changes in the heart rate, an effect mediated by the area postrema.

In one example, experiments done by Bernstein et al. on rats indicated that the area postrema lesions prevented the detection of lithium chloride, which can become toxic at high concentrations.

In addition to simple taste aversions, rats with the area postrema lesions failed to perform other behavioral and physiological responses associated with the introduction of the toxin and present in the control group, such as lying down on their bellies, delayed stomach emptying, and hypothermia.

Stimulation of the dopamine receptors in the area postrema activates these vomiting centers of the brain; this is why nausea is one of the most common side-effects of antiparkinsonian drugs.

[14] The area postrema was first named and located in the gross anatomy of the brain by Magnus Gustaf Retzius, a Swedish anatomist, anthropologist and professor of histology.

The area postrema had been anatomically identified and named nearly 60 years earlier, but its function had remained unknown until its role in emesis was later confirmed.

[18] A 2009 study followed the development of the area postrema, using a macaque monkey model in an attempt to identify and characterize neurotransmission in this region as well as to resolve outstanding incongruities across research.

These scientists found, in culmination, that previous studies suggest noradrenalin and/or dopamine cause CA fluorescence in the area postrema macaque-CA, meaning catecholaminergic or derived from an amine and functioning as a neurotransmitter or hormone or both.

A particular mechanism, employed by the drug pramlintide, acts mainly on the area postrema and results in decreased glucagon secretion, which in turn slows down gastric emptying and the satiety effect.

[22][23] The mechanism for this physiological reaction is still not fully understood, but the area postrema's ability to regulate cardiovascular function presents a very interesting direction for neuroendocrinology.