Ondansetron prevents chemotherapy-induced nausea but has no effect on motion sickness. The receptor selectivity that explains this clinical difference is:

• A Ondansetron blocks dopamine D2 receptors in the CTZ but not vestibular end organ dopamine receptors
• B Ondansetron blocks 5-HT3 receptors in the GIT and CTZ but not the histamine H1 and muscarinic M1 receptors in the vestibular pathway ✓
• C Ondansetron inhibits NK1 receptors in the nucleus tractus solitarius but lacks effect on vestibular GABA receptors
• D Ondansetron has no access to the blood-brain barrier, limiting its effect to peripheral 5-HT3 receptors

Explanation

Chemotherapy-induced nausea is primarily mediated by 5-HT released from enterochromaffin cells stimulating vagal afferents (5-HT3 receptors) and directly activating the chemoreceptor trigger zone (CTZ). Ondansetron blocks 5-HT3 receptors at both sites. Motion sickness, however, is mediated by conflicting vestibular signals processed via histaminergic (H1) and muscarinic (M1) pathways in the cerebellum and brainstem — receptors not blocked by ondansetron. Antihistamines (cyclizine) and anticholinergics (scopolamine) are effective for motion sickness.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.