Sensibility Of Estrogen Receptors On Susceptibility Of Motion Sickness

Motion sickness (MS) is a result of the body exposed to passive movement environment, causing orientation and body balance dysfunction, with severe vestibular and autonomic reaction. There may be dizziness, headache, cold sweats, pale, nausea, vomiting syndrome that can be too serious to loss of self-care ability or operational capacity, or systemic dehydration and disturbance of electrolyte balance.The pathogenesis of motion sickness has been not yet fully understood. Motion sickness is considered with the integration of vestibular stimulation, visual perception stimulation and proprioception stimulation. Since 1950's, there were more than ten of theories or hypotheses on the pathogenesis of motion sickness. Most scholars accepted the "Sensory Conflict Hypothesis" or "Neural Mismatch Hypothesis".Many research findings have reported that women are more susceptible to motion sickness than men. Why is the motion sickness susceptibility gender-related? What is the pathophysiological mechanism? What is associated with the sex hormone and its receptor?There is no systematic study on these questions. According to the present subject classification, motion sickness and female hormones, especially estrogen, is two difficult issues to link. Carrying out research on this subject, can provide new understanding on etiology of motion sickness, and has important practical significance.Objective:Combination of mouse hot-plate motion sickness model and rat "pica" motion sickness model, try to find the relationship between estrogen and motion sickness, and use another motion sickness model: mouse gastric emptying model for comprehensive observation of their relationship. By using different motion sickness model, check the effect of estrogen receptor agonists or antagonist on mouse or rat's motion sickness indicators. By using semi-quantitative RT-PCR, check the expression of estrogen receptors mRNA at different part of brain,study the change of estrogen receptors when got motion sickness. According the above experiment,provide experimental basis in laboratory on "Hypothesis on susceptibility of motion sickness mediated by estrogen".Methods and Results:1 Effects of estrogen on susceptibility of motion sicknessThe rodents were received the following treatment: surgical castration, chemical castration (treated with estrogen receptor antagonist), feminization of male animals and females were treated with artificial maintenance of estrous cycle. By using these animal models, the effects of estrogen on susceptibility of motion sickness were checked.The results showed that females had stronger reaction than males on motion sickness. Compared with normal females, the females which were treated with surgical castration and chemical castration had lower reaction of motion sickness. But the animals which were treated with feminization and artificial maintenance of estrous cycle had no different with the normal females. By given estrogen receptorαagonists, we found that there were no different between estrogen receptor agonists and estrogen on motion sickness. But when given estrogen receptorβagonists, we found that it had different effects on different models. On mouse rotation-hot-plate motion sickness model, estrogen receptorβagonists had no different effects with estrogen; on mouse gastric emptying motion sickness model, it strengthened the reaction of motion sickness; on rat pica motion sickness model, it inhibited the reaction of motion sickness. So we need more experiments on molecular level to verify the effect of estrogen receptorβagonists on motion sickness.2 The level of estrogen receptor mRNA expression on motion sicknessBy checking the level of estrogen receptor mRNA expression on hypothalamic, cortex and cerebella after rotation, the results would provide direct support on the effects estrogen on susceptibility of motion sickness.The results showed as following: first on the mouse models, compared with the control group, there were expression of ERαand ERβon hypothalamic and cerebella after rotation, without on cortex. And the expression of ERαhad significant difference with ERβon hypothalamic,ERαhad more expression. On rat model, compared with the control group, there were more expression of ERαon hypothalamic, without expression of ERβon hypothalamic before or after rotation. According to the results, we speculate that ERαis more important to the effects of estrogen on susceptibility of motion sickness.Conclusion:There are relationship between estrogen and motion sickness. Higher level of estrogen, more serious reactions motion sickness will be. Hypothalamic and cerebella have important role on the regulation of estrogen to motion sickness, and hypothalamic is more important. ERαplays a major role on the regulation of estrogen to motion sickness.