Morita M
Nihon Jibiinkoka Gakkai Kaiho. 1989 Sep;92(9):1424-35. doi: 10.3950/jibiinkoka.92.1424.
Complex accelerative stimuli can induce pica in rats as well as the treatment with poisons, which means eating of non-nutritive substances such as kaolin, in proportion to the severity of their sickness. For the purpose of using pica as an index of motion sickness in rats, we examined what kind of rotation was effective for inducing pica in rats with or without normal bilateral labyrinth functions. Clinically potent anti-motion sickness drugs, such as scopolamine, methamphetamine, diphenhydramine, were examined in reducing rotation-induced pica in rats. Rats ate more kaolin after double rotation with continuously changing acceleration, than after single rotation. Both the animals treated with anti-motion sickness drugs or labyrinthectomy ate less kaolin even after double rotation. Since the physiological and pharmacological mechanisms for inducing pica in rats were similar with those of motion sickness in humans, pica in rats should be an acceptable index of their motion sickness. In order to study neural mechanisms of motion sickness in rats, we examined the effects of an anti-cholinergic as a potent anti-motion sickness drug and cholinergics as an antagonistic drug treated during the 4th-7th day of rotation on both habituation to double rotation within daily rotations for 10-11 days, using pica as an index of motion sickness. Rats were separated into three groups according to their initial susceptibility, and rats with low susceptibility were omitted in these experiments. Scopolamine (TTS-scopolamine) as an anticholinergic facilitated habituation to motion, especially in rats with moderate susceptibility. Treatment of physostigmine suppressed residual habituation to motion sickness in rats, especially with moderate susceptibility, though neostigmine, peripherally acting anti-cholinesterase, had no effect. These results suggested that centrally acting acetylcholine play an important role in suppressing habituation of motion sickness. In conclusion, rats should be a convenient model for studying for motion sickness, as we examined one of the neural mechanisms in motion sickness using pica as an index.
复杂的加速刺激以及用毒物处理均可诱发大鼠异食癖，即大鼠会根据病情严重程度食用高岭土等非营养性物质。为了将异食癖用作大鼠晕动病的指标，我们研究了何种旋转方式对有或无正常双侧迷路功能的大鼠诱发异食癖有效。我们还检测了临床上有效的抗晕动病药物，如东莨菪碱、甲基苯丙胺、苯海拉明，对减少大鼠旋转诱发异食癖的作用。与单次旋转相比，大鼠在持续改变加速度的双次旋转后食用了更多高岭土。接受抗晕动病药物治疗或迷路切除的动物，即使在双次旋转后食用的高岭土也较少。由于大鼠诱发异食癖的生理和药理机制与人类晕动病相似，大鼠的异食癖应是其晕动病的一个可接受指标。为了研究大鼠晕动病的神经机制，我们以异食癖作为晕动病指标，检测了在第4至7天旋转期间使用强效抗晕动病药物抗胆碱能药物以及作为拮抗药物的胆碱能药物，对10至11天每日旋转中双次旋转习惯化的影响。根据大鼠的初始易感性将其分为三组，在这些实验中剔除了低易感性的大鼠。作为抗胆碱能药物的东莨菪碱（经皮东莨菪碱）促进了对运动的习惯化，尤其是在中度易感性的大鼠中。毒扁豆碱治疗抑制了大鼠对晕动病的残余习惯化，尤其是在中度易感性的大鼠中，而外周作用的抗胆碱酯酶新斯的明则没有效果。这些结果表明，中枢作用的乙酰胆碱在抑制晕动病习惯化中起重要作用。总之，大鼠应是研究晕动病的便利模型，因为我们以异食癖为指标研究了晕动病的一种神经机制。
