title: 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 modifying the neural store to facilitate the acquisition of habituation to provocative motion.
authors.affiliation: Department of Otolaryngology, Osaka University Medical School, Japan.
authors.forename: N
authors.initials: N
authors.lastname: Takeda
authors.forename: M
authors.initials: M
authors.lastname: Morita
authors.forename: S
authors.initials: S
authors.lastname: Hasegawa
authors.forename: A
authors.initials: A
authors.lastname: Horii
authors.forename: T
authors.initials: T
authors.lastname: Kubo
authors.forename: T
authors.initials: T
authors.lastname: Matsunaga
mesh_terms: D000818:Animals; D001921:Brain / Q000503:physiopathology*; D009041:Motion Sickness / Q000503:physiopathology*; D009480:Neuropharmacology; D051381:Rats; D011969:Receptors, Histamine H1 / Q000187:drug effects / Q000502:physiology*; D012018:Reflex / Q000502:physiology; D014839:Vomiting / Q000503:physiopathology*
chemical_list: D011969:Receptors, Histamine H1