2022 Volume 158 Pages 62-71
The neural mismatch hypothesis is widely accepted to explain the development of motion sickness. Essential to the neural mismatch hypothesis of motion sickness is the neural mismatch signal encoding spatial disorientation. We examined the neurochemical response to caloric stimulation with hot or cold water in the rat brain. Caloric stimulation with hot or cold water induced biphasic release of glutamate in the vestibular nucleus, indicating that the vestibular input is directly transmitted from the inner ear to the vestibular nucleus. However, hot or cold caloric stimulation induced monophasic release of histamine and acetylcholine in the hypothalamus and hippocampus respectively, suggesting that the neural mismatch signal, but not vestibular input itself, is transmitted to these regions. Our previous study showed that the hypothalamus plays an important role in the vestibule-autonomic reflex. Since the hippocampus has a spatial map, the possibility that the hippocampus generates the neural mismatch signal was examined. In our lesion study using a rat model, the hippocampal lesion aggravated motion sickness, suggesting that the hippocampus counteracts spatial disorientation. On the other hand, the cerebellar lesion had no effect on the development of motion sickness, suggesting that the cerebellum is not the origin of the neural mismatch signal.
