Motion Sickness Induces Intestinal Transit Increase in Mice

Motion sickness in rodents could be induced with vestibular stimulation from rotation [1]. However, rats and mice could not nauseate and vomit due to the powerful barrier between the stomach and the esophagus [2]. Instead, they exhibit pica behavior (eating of kaolin), which has already been thought as an alternative to nausea and vomiting in rats [3]. Nonetheless, no significant increase in kaolin consumption after rotation was observed in mice [4,5]. We speculated that the amount of kaolin consumption induced by rotation is too little to distinguish from that due to the curious habit in mice. Furthermore, the biological basis of pica induced by motion sickness in rodents is still unknown. Recently, motion sickness index (MSI), fecal-based evaluation criteria, was verified to be suitable for evaluating the severity of motion sickness in mice [4,6]. The results indicated that intestinal transit may increase when mice suffer from motion sickness. On the other hand, it was demonstrated that space motion sickness could result in gastric stasis in astronauts [7]. How to clarify this conflict? We presume that the gastric stasis does exist in mice after rotary stimulus, and then, the intestinal transit is increased to resist gastric stasis instead of emesis. Moreover, in our previous study, we found that fecal granules determined MSI score to a great extent. Therefore, there may be a correlation between intestinal transit and MSI. The present work was therefore designed to investigate intestinal transit variation during motion sickness and the correlation between intestinal transit and MSI in mice. C57BL/6J male mice weighing 18–22 g were purchased from SLRC Laboratory Animal Ltd (Shanghai, China). All animals received humane care, and experimental procedures were in compliance with institutional animal care guidelines. Motion sickness was induced by biaxial rotary stimulus with 360°/s peak velocity and 20°/s angular accelerative rotation for 40 min. MSI was calculated on the basis of a set of evaluation criteria previously published [4]. Kaolin consumption in 24 h prerotation or postrotation was recorded. Small intestinal transit and colonic transit activity were determined using 10% wood charcoal mixing 5% gum arabic as tracer dye. The ratio of distance from pylorus to the end of tracer dye and distance from pylorus to cecum was identified as small intestinal transit activity. The ratio of distance from ileocecal junction to the end of tracer dye to total length of colon was identified as colonic transit activity [8]. Data are expressed as mean SD. Comparisons of parameters among two groups were made by the unpaired Student’s t-test. Data involving more than two groups were assessed by analysis of variance (ANOVA). Statistical significance was set at P < 0.05. Liu et al. [9] reported mice ate a small amount of kaolin in normal condition (<0.2 g each day). In our experiment, kaolin consumption before and after rotary stimulus was 0.35 0.61 and 0.38 0.54 g in 24 h, respectively. Moreover, among 42 mice, 57.1% showed increased kaolin consumption after rotary stimulus. Inversely, 42.9% exhibited decreased kaolin consumption. Taken together, the results indicated that the basic consumption of kaolin is little, and the variability of kaolin consumption is huge in mice. Our results showed that pica is not suitable to evaluate the severity of motion sickness in mice. In normal condition, the intestinal transit was increased with time after intragastric administration of tracer dye (data not