Journal
ACTA OTO-LARYNGOLOGICA
Volume 129, Issue 1, Pages 45-51Publisher
TAYLOR & FRANCIS AS
DOI: 10.1080/00016480802008173
Keywords
Motion sickness; histamine; H1 receptor; kaolin; mepyramine; terfenadine; zolantidine; hypothalamus; brainstem
Categories
Funding
- Ministry of Education, Science, Sports, and Culture of Japan
- Health and Labor Science Grants in Japan
Ask authors/readers for more resources
Conclusion: The study findings suggest that histamine was released from the axon terminals in the hypothalamus and brainstem and the released histamine activated post-synaptic H1 receptors there, resulting in the development of motion sickness. Objectives: We first examined which subtype of post-synaptic histaminergic receptor was responsible for the development of motion sickness. We then examined whether H1 receptors were up-regulated in various areas of the rat brain after 2 G hypergravity load, because the stimulation of H1 receptor was reported to up-regulate the level of H1 receptor protein expression through augmentation of H1 receptor mRNA expression. Materials and methods: For this purpose, we used an animal model of motion sickness, using pica (eating non-nutritive substances such as kaolin), as a behavioral index in rats. Results: After 2 G hypergravity load, rats ate a significant amount of kaolin, indicating that they suffered from motion sickness. The hypergravity-induced kaolin intake was suppressed by mepyramine, but not by terfinadine or zolantizine. This finding indicates that cerebral post-synaptic H1 but not H2 or peripheral H1 receptors play an important role in the development of motion sickness. The expression of H1 receptor mRNA was up-regulated in the hypothalamus and brainstem, but not in the cerebral cortex after 2 G hypergravity load in rats.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available