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The involvement of 5-HT3 and 5-HT4 receptors in anticancer drug-induced emesis

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—Emesis caused by cytotoxic drugs is associated with an increase in the concentration of serotonin (5-hydroxytryptamine: 5-HT) in the intestine and the brainstem. 5-HT receptors in the central nervous system (CNS) and the gut participate in the induction of emesis. 5-HT1 receptors are negatively coupled to adenylate cyclase, but the 5-HT2C subtype is linked to phospholipase (PL) C activation. The 5-HT4 receptor, by contrast, is positively coupled to adenylate cyclase. 5-HT1A and 5-HT2A /5-HT2C agonists exhibit antiemetic properties. The 5-HT1D agonist reduces the emesis accompanying migraine headaches. Through use of 5-HT3 receptor antagonists, which selectively antagonize 5-HT3 receptors on the abdominal vagal afferent fibers, as much as 60% of the initial emetic response can be prevented. Inhibition of acute emesis also appears to be attained by blocking the initiation of the emetic reflex induced via 5-HT3 receptors by 5-HT released from enterochromaffin (EC) cells in the small intestine. Although 5-HT4 receptor antagonists have an antiemetic activity in some experimental models, the precise role of 5-HT4 receptors has not been fully elucidated. The present review aims to compare the involvement of 5-HT4 receptors with that of the 5-HT3 receptors in anticancer drug-induced emesis.


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