Signal cording and target net work of spatial disorientation in the brain

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We have developed an animal model of motion sickness, using pica as a behavioral index of motion sickness in rats. Rats cannot vomit, but pica, the ingestion of non-nutritive substances such as kaolin (hydrated aluminum silicate), is an illness-response behavior, which is analogous to vomiting. After 2-hours load of 2g hypergravity, rats ate a significant amount of kaolin, indicating that they suffered from motion sickness. The hypergravity-induced kaolin intake was suppressed by mepyramine, an H1 antagonist, but not by zolantizine, an H2 antagonist. A 2-h load of 2g hypergravity also transiently increased the release of histamine in the rat hypothalamus measured by in vivo brain microdialysis. These findings suggested that the activation of the central histaminergic neuron systems after hypergravity induces motion sickness via H1 receptors (H1R).Then, to investigate changes in post-synaptic events in the development of motion sickness, gene expression of H1R in the rat hypothalamus was examined using a real-time PCR method after hypergravity. The expression of H1R mRNA in the rat hypothalamus was significantly increased after 2g hypergravity for 2 hours, indicating an up-regulation of H1R induced by hypergravity. Taken together with the previous finding demonstrating an activation of the histaminergic neurons after hypergravity, the present finding further indicate an amplification of the H1 transmission in the development of motion sickness,. The up-regulation of H1R may contribute to the built up characteristic of motion sickness symptoms, which developed gradually at first and then progressed rapidly.