Abstract

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.

Highlights

  • Motion sickness is a common and challenging problem

  • Administration of anisodamine decreased the expression of calcitonin gene-related peptide (CGRP) within the vestibular efferent nucleus and the vestibular nucleus in rats subjected to rotary stimulation

  • CGRP possibly plays a role in motion sickness and its mechanism merits further investigation

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Summary

Introduction

Motion sickness is a common and challenging problem. Various physiological measurements for this problem have been tested. [1,2,3,4] It is well known that a functioning vestibular system is essential for the perception of motion sickness. The innervations of the vestibular system include both the afferent and efferent vestibular system (EVS). Vestibular sensory organs in the inner ear are innervated by true efferent fibers originating from brainstem neurons. Studies show that electrical stimulation of EVS fibers can result in both facilitatory and inhibitory modulation of the sensory activity in the afferent vestibular system. [6] EVS is considered to play a role in the modulation of the afferent input from the peripheral vestibular receptors to the central nervous system. Studies show that electrical stimulation of EVS fibers can result in both facilitatory and inhibitory modulation of the sensory activity in the afferent vestibular system. [6] EVS is considered to play a role in the modulation of the afferent input from the peripheral vestibular receptors to the central nervous system. [7]

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