Neuropharmacology of Motion Sickness and Emesis: A review

Abstract

Histamine H₁-receptors are involved in the development of the symptoms and signs of motion sickness, including emesis. On provocative motion stimulus, a signal for sensory conflict activates the histaminergic neuron system, and the histaminergic descending impulse stimulates H₁-receptors in the emetic center of the brain stem. The histaminergic input to the emetic center through H₁-receptors is independent of dopamine D₂-receptors in the chemoreceptor trigger zone and serotonin 5HT₃-receptors in the visceral afferent, which are also involved in the emetic reflex. Antihistamines block emetic H₁-receptors to prevent motion sickness. Acetylcholine muscarinic receptors are involved in the generation of signals for sensory conflict. Anti-cholinergic drugs prevent motion sickness by modifing the neural store to facilitate the acquisition of habituation to provocative motion.

Key Words:

• histamine H₁-receptor
• acetylcholine muscarinic receptor
• dopamine D₂-receptor
• serotonin 5HT₃-receptor
• pica
• rat.