Sato Go, Uno Atsuhiko, Horii Arata, Umehara Hayato, Kitamura Yoshiaki, Sekine Kazunori, Tamura Koichi, Fukui Hiroyuki, Takeda Noriaki
Department of Otolaryngology, Institute of Health Biosciences, University of Tokushima Graduate School, 3-18-15 Kuramoto, Tokushima, Japan.
Acta Otolaryngol. 2009 Jan;129(1):45-51. doi: 10.1080/00016480802008173.
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.
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.
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.
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.
研究结果表明，组胺从下丘脑和脑干的轴突终末释放，释放的组胺激活了那里的突触后H1受体，导致晕动病的发生。
我们首先研究哪种突触后组胺能受体亚型与晕动病的发生有关。然后，我们研究了在2G超重力负荷后大鼠脑的各个区域中H1受体是否上调，因为据报道H1受体的刺激通过增加H1受体mRNA表达来上调H1受体蛋白表达水平。
为此，我们使用了一种晕动病动物模型，以异食癖（食用高岭土等非营养物质）作为大鼠的行为指标。
在2G超重力负荷后，大鼠食用了大量高岭土，表明它们患有晕动病。苯海拉明可抑制超重力诱导的高岭土摄入，但特非那定或左西替利嗪则不能。这一发现表明，大脑突触后H1受体而非H2受体或外周H1受体在晕动病的发生中起重要作用。在大鼠2G超重力负荷后，下丘脑和脑干中H1受体mRNA的表达上调，但大脑皮层中未上调。
