Neural mechanisms of motion sickness.
Three kinds of neurotransmitters: histamine, acetylcholine and noradrenaline, play important roles in the neural processes of motion sickness, because antihistamines, scopolamine and amphetamine are effective in preventing motion sickness. Histamine H1-receptors are involved in the development of the symptoms and signs of motion sickness, including emesis. On provocative motion stimuli, a neural mismatch signal activates the histaminergic neuron system in the hypothalamus, and the histaminergic descending impulse stimulates H1-receptors in the emetic center of the brainstem. The histaminergic input to the emetic center through H1-receptors is independent of dopamine D2-receptors in the chemoreceptor trigger zone in the area postrema 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. Scopolamine prevents motion sickness by modifying the neural store to reduce the neural mismatch signal and by facilitating the adaptation/habituation processes. The noradrenergic neuron system in the locus coeruleus is suppressed by the neural mismatch signal. Amphetamine antagonizes mismatch-induced suppression of noradrenergic neural transmission, resulting in preventing motion sickness.
Takeda
N
N
Department of Otolaryngology, University of Tokushima School of Medicine, Kuramoto-cho, Tokushima 770-8503, Japan.
Morita
M
M
Horii
A
A
Nishiike
S
S
Kitahara
T
T
Uno
A
A
D000818:Animals; D004198:Disease Susceptibility; D006801:Humans; D009041:Motion Sickness / Q000209:etiology / Q000378:metabolism* / Q000517:prevention & control / Q000628:therapy; D009474:Neurons / Q000378:metabolism*; D015398:Signal Transduction / Q000502:physiology*