A novel animal model for motion sickness and its first application in rodents

Yu, Xuhong; Cai, Guo-Jun; Liu, Aijun; Chu, Zun-hua; Su, Ding‐Feng

doi:10.1016/j.physbeh.2007.05.067

Cited by 37 publications

(41 citation statements)

References 19 publications

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“…A recent paper reported an animal model of motion sickness using mice and rats by rotating animals for 40 min (Yu et al, 2007). However, autonomic disturbances were not investigated in the present study since 3 laps of backward translocation lasted only for about 10 min in the present study.…”

Section: Sensory Mismatch In the Backward Conditionmentioning

confidence: 74%

Rat hippocampal theta rhythm during sensory mismatch

et al. 2008

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It has been suggested that sensory mismatch induces motion sickness, but its neural mechanisms remain unclear. To investigate this issue, theta waves in the hippocampal formation (HF) were studied during sensory mismatch by backward translocation in awake rats. A monopolar electrode was implanted into the dentate gyrus in the HF, from which local field potentials were recorded. The rats were placed on a treadmill affixed to a motion stage translocated along a figure 8-shaped track. The rats were trained to run forward on the treadmill at the same speed as that of forward translocation of the motion stage (a forward condition) before the experimental (recording) sessions. In the experimental sessions, the rats were initially tested in the forward condition, and then tested in a backward (mismatch) condition, in which the motion stage was turned around by 180 degrees before translocation. That is, the rats were moved backward by translocation of the stage although the rats ran forward on the treadmill. The theta (6-9 Hz) power was significantly increased in the backward condition compared with the forward condition. However, the theta power gradually decreased by repeated testing in the backward condition. Furthermore, backward translocation of the stage without locomotion did not increase theta power. These results suggest that the HF might function as a comparator to detect sensory mismatch, and that alteration in HF theta activity might induce motion sickness.

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Section: Sensory Mismatch In the Backward Conditionmentioning

confidence: 74%

Rat hippocampal theta rhythm during sensory mismatch

et al. 2008

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“…Comparison of the data for scopolamine from in vivo studies in rats (Morita et al, 1988; Yu et al, 2007) led us to select a dose of 10 mg/kg, which we considered sufficient to block muscarinic receptors (10 times lower than in the original studies) (Ueno et al, 1988). …”

Section: Discussionmentioning

confidence: 99%

Brain Activation by H1 Antihistamines Challenges Conventional View of Their Mechanism of Action in Motion Sickness: A Behavioral, c-Fos and Physiological Study in Suncus murinus (House Musk Shrew)

Dieser

et al. 2017

Front. Physiol.

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Motion sickness occurs under a variety of circumstances and is common in the general population. It is usually associated with changes in gastric motility, and hypothermia, which are argued to be surrogate markers for nausea; there are also reports that respiratory function is affected. As laboratory rodents are incapable of vomiting, Suncus murinus was used to model motion sickness and to investigate changes in gastric myoelectric activity (GMA) and temperature homeostasis using radiotelemetry, whilst also simultaneously investigating changes in respiratory function using whole body plethysmography. The anti-emetic potential of the highly selective histamine H1 receptor antagonists, mepyramine (brain penetrant), and cetirizine (non-brain penetrant), along with the muscarinic receptor antagonist, scopolamine, were investigated in the present study. On isolated ileal segments from Suncus murinus, both mepyramine and cetirizine non-competitively antagonized the contractile action of histamine with pKb values of 7.5 and 8.4, respectively; scopolamine competitively antagonized the contractile action of acetylcholine with pA2 of 9.5. In responding animals, motion (1 Hz, 4 cm horizontal displacement, 10 min) increased the percentage of the power of bradygastria, and decreased the percentage power of normogastria whilst also causing hypothermia. Animals also exhibited an increase in respiratory rate and a reduction in tidal volume. Mepyramine (50 mg/kg, i.p.) and scopolamine (10 mg/kg, i.p.), but not cetirizine (10 mg/kg, i.p.), significantly antagonized motion-induced emesis but did not reverse the motion-induced disruptions of GMA, or hypothermia, or effects on respiration. Burst analysis of plethysmographic-derived waveforms showed mepyramine also had increased the inter-retch+vomit frequency, and emetic episode duration. Immunohistochemistry demonstrated that motion alone did not induce c-fos expression in the brain. Paradoxically, mepyramine increased c-fos in brain areas regulating emesis control, and caused hypothermia; it also appeared to cause sedation and reduced the dominant frequency of slow waves. In conclusion, motion-induced emesis was associated with a disruption of GMA, respiration, and hypothermia. Mepyramine was a more efficacious anti-emetic than cetirizine, suggesting an important role of centrally-located H1 receptors. The ability of mepyramine to elevate c-fos provides a new perspective on how H1 receptors are involved in mechanisms of emesis control.

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“…However, the utility and broad acceptance of these newer indices may require further investigation. [20] Compared to observing symptoms and Pica, CTA is sensitive, simple, stable, easy to perform, and applicable to a variety of animals. Furthermore, CTA is readily quantifiable and, consequently, more commonly used.…”

Section: Discussionmentioning

confidence: 99%

Expression of Calcitonin Gene-Related Peptide in Efferent Vestibular System and Vestibular Nucleus in Rats with Motion Sickness

et al. 2012

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Motion sickness presents a challenge due to its high incidence and unknown pathogenesis although it is a known fact that a functioning vestibular system is essential for the perception of motion sickness. Recent studies show that the efferent vestibular neurons contain calcitonin gene-related peptide (CGRP). It is a possibility that the CGRP immunoreactivity (CGRPi) fibers of the efferent vestibular system modulate primary afferent input into the central nervous system; thus, making it likely that CGRP plays a key role in motion sickness. To elucidate the relationship between motion sickness and CGRP, the effects of CGRP on the vestibular efferent nucleus and the vestibular nucleus were investigated in rats with motion sickness.MethodsAn animal model of motion sickness was created by subjecting rats to rotary stimulation for 30 minutes via a trapezoidal stimulation pattern. The number of CGRPi neurons in the vestibular efferent nucleus at the level of the facial nerve genu and the expression level of CGRPi in the vestibular nucleus of rats were measured. Using the ABC method of immunohistochemistry technique, measurements were taken before and after rotary stimulation. The effects of anisodamine on the expression of CGRP in the vestibular efferent nucleus and the vestibular nucleus of rats with motion sickness were also investigated.Results and DiscussionBoth the number of CGRPi neurons in the vestibular efferent nucleus and expression level in the vestibular nucleus increased significantly in rats with motion sickness compared to that of controls. The increase of CGRP expression in rats subjected to rotary stimulation 3 times was greater than those having only one-time stimulation. Administration of anisodamine decreased the expression of CGRP within the vestibular efferent nucleus and the vestibular nucleus in rats subjected to rotary stimulation. In conclusion, CGRP possibly plays a role in motion sickness and its mechanism merits further investigation.

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A novel animal model for motion sickness and its first application in rodents

Cited by 37 publications

References 19 publications

Rat hippocampal theta rhythm during sensory mismatch

Rat hippocampal theta rhythm during sensory mismatch

Brain Activation by H1 Antihistamines Challenges Conventional View of Their Mechanism of Action in Motion Sickness: A Behavioral, c-Fos and Physiological Study in Suncus murinus (House Musk Shrew)

Expression of Calcitonin Gene-Related Peptide in Efferent Vestibular System and Vestibular Nucleus in Rats with Motion Sickness

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