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.
2008-12-19
Eng.
Department of Otolaryngology, Institute of Health Biosciences, University of Tokushima Graduate School, 3-18-15 Kuramoto, Tokushima, Japan. go-sato [at] clin.med.tokushima-u.ac.jp
Acta Otolaryngol. 2009 Jan;129(1):45-51
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