Central neurologic control of vomiting involves two anatomically and functionally separate units; the VC or emetic center and the CTZ.
Notes: The CTZ lies outside the BBB and is responsive to circulating emetogens. These emetogenic stimuli act either peripherally by stimulating vagal or sympathetic afferents or centrally by stimulation of the CTZ. All stimuli are mediated through the VC, regardless of the cause. The VC integrates efferent input from a number of sources including the cerebral cortex (psychogenic vomiting), vestibular input arising from the semicircular canals (vomiting associated with motion sickness or vestibular disorders), vagal and sympathetic fibers, especially from the gastrointestinal system, and the CTZ. Key neurotransmitter receptors involved in the emetic response include: serotonin (5-HT), NK-1, dopamine (D2), histamine (H1), cholinergic (ACh), and mu opioid. Since stimulant pathways converge at the level of the VC, effective blocking of the vomiting reflex at this level is effective in preventing emesis, whether it is generated centrally or peripherally.
Abbreviations: ACh, acetylcholine; BBB, blood–brain barrier; CTZ, chemoreceptor trigger zone; GABA, gamma amino butyric acid; NK-1, neurokinin-1; VC, vomiting center.