Neuropharmacology of motion sickness and emesis. A review.
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.
Takeda
N
N
Department of Otolaryngology, Osaka University Medical School, Japan.
Morita
M
M
Hasegawa
S
S
Horii
A
A
Kubo
T
T
Matsunaga
T
T
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*
D011969:Receptors, Histamine H1