Stimuli Arising from the Area Postrema Related Areas

It was established nearly 100 years ago that the application of chemicals to the dorsal surface of the brainstem or the ventricular system could induce emesis. In these early studies it was assumed that this

Figure 2 The stimuli causing chemo- and mechanoreceptors for stimulation of the vagus and splanchnic nerves in the gut wall to induce nausea and emesis. An inflammatory response may damage cellular elements leading to the release of prostaglandins and kinins which may stimulate the enterochromaoffin cells (EC) or possibly platelets. This will cause the release of serotonin, which may activate 5-HT3 receptors located on the vagus nerve to trigger the emetic reflex.

Figure 2 The stimuli causing chemo- and mechanoreceptors for stimulation of the vagus and splanchnic nerves in the gut wall to induce nausea and emesis. An inflammatory response may damage cellular elements leading to the release of prostaglandins and kinins which may stimulate the enterochromaoffin cells (EC) or possibly platelets. This will cause the release of serotonin, which may activate 5-HT3 receptors located on the vagus nerve to trigger the emetic reflex.

occurred through a "vomiting center'' in the brain stem. Again, it was the studies of Borison and colleagues that showed that a number of stimuli were actually detected by cells in the caudal part of the floor of the fourth ventricle, the area postrema, which was termed a "chemoreceptor trigger zone'' for emesis. The area postrema is a circumventricular organ of the brain outside the blood-brain barrier, with the capillaries within the area lacking endothelial occluding junctions. Also, the ventricular ependymal cells lack occluding junctions, making the structure permeable to molecules in the blood or ventricles to provide an efficient chemoreceptor sensor for numerous chemicals and endogenous substances (Fig. 4).

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