Prevention and treatment of motion sickness is a challenge, particularly in aerospace medicine, due to its high incidence and unclear pathogenesis. At present, animal models of motion sickness have been developed in cats, dogs, rats, and squirrel monkeys. CTA and pica are classic indices to evaluate the animal model of motion sickness. CTA, a significant decrease in the animals' consumption of some substance with a certain taste (e.g., saccharin solution), can be induced by various stimuli. Pica, an increase in the animals' consumption of kaolin or other substances of no nutritional value, can also be induced. Today, CTA is extensively used to evaluate the animal model of motion sickness by observing the decrease in consumption of saccharin solution after stimulation, while pica is used by observing the increase in consumption of kaolin after stimulation. Recent studies suggest other new indices for the study of motion sickness by observing symptoms after rotation, such as piloerection, tremble, urinal and fecal incontinence. However, the utility and broad acceptance of these newer indices may require further investigation. 
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. Moreover, CTA is a behavioral index that, through the degree of antidipsia, reflects the severity of motion sickness. 
Therefore, in our experiments, we observe the changes in the intake volumes of saccharin solution before and after rotation to evaluate the animal model of motion sickness in rats. The intake volume of 0.15% saccharin solution was significantly reduced after motion stimulation. Antidipsia can be decreased by administration of anisodamine – an anticholinergic drug currently used to prevent and treat motion sickness. Observation of this effect further indicates the validity of our animal model using rotary stimulation for 30 minutes in a trapezoidal pattern.
The efferent vestibular neurons (EVN) are located in the vestibular efferent nucleus (VEN) and are mainly composed of 3 types of neurons – DL, M, and CPR. Many of the EVN are CGRPi and send efferent fibers to the vestibular end-organs. 
In our experiments, the number of CGRPi neurons in VEN increased significantly in rats after rotary stimulation. Moreover, the increase of CGRPi neurons in rats after rotary stimulus was 3 times greater than that of the rats that underwent rotary stimulus only once.
The exact role of CGRP in EVS still is unclear today, but it has been found that CGRP increases the discharge firing rate of afferent fibers innervating the hair cells in the lateral line organ of Xenopus laevis. 
In end-organs of the human vestibule, CGRPi is located in vesiculated nerve fibers and bouton-type nerve terminals that directly contact afferent nerve chalices surrounding type I sensory cells and afferent nerve fibers to form an en passant
contact with afferent dendrites. 
It follows that the release of CGRP is able to directly alter primary afferent inputs via type I hair cells of the central vestibular nervous system. On the other hand, EVN contain both CGRP and choline acetyltransferase; and studies have found an interaction between CGRP and acetylcholine. 
The acetylcholine-mediated efferent system is thought to provide a tonic inhibitory influence on the afferent activity arising from each vestibular receptor. Although such an interaction is not clear in the vestibular system, it has been reported that CGRP increases intracellular Ca2+
concentration in response to Ach in cochlear hair cells. 
CGRP has also been shown to influence the expression of nicotinic acetylcholine receptor (nAChR) subunits in skeletal muscle which leads to an increase in cAMP levels and acetylcholine receptor synthesis. CGRP may have a similar regulatory role in the vestibular system. 
CGRP up-regulates synthesis of acetylcholine receptors and alters the sensitivity of primary afferent neurons to acetylcholine.
Recently, researchers report that the vestibular nuclei contain numerous afferent neurons that send projections to the vestibular efferent nucleus, some of which are CGRP cells. 
This afferent innervation provides morphological evidence that EVN receive input from including CGRP cells. 
These vestibular primary CGRP afferent neurons may have an influence on EVN. CGRP acts as an important co-transmitter and modulator in the afferent-mediated activity of vestibular efferent neurons, which in turn affect afferents in the vestibular end-organs. 
In our study, we observe that the level of CGRP fiber immunoreactivity in the vestibular nucleus increases significantly in an animal model of motion sickness, and the increase after 3 rotary stimulation events is greater than after rotary stimulation once. It is unclear today whether the CGRP fibers are afferent to the vestibular efferent nucleus from CGRP afferent cells in the vestibular nucleus or efferent from VEN to the vestibular nucleus. However, the results of our current studies suggest that CGRP may have a potential role in motion sickness.
In our experiments, the number of CGRPi neurons in VEN and the level of CGRP fiber immunoreactivity in the vestibular nucleus increased significantly in rats following rotary stimulation. Our findings have provided further evidence to indicate an important role of CGRP in the pathogenesis of motion sickness and support additional neurophysiological and molecular biological studies.
Anisodamine and scopolamine are anti-cholinergic drugs and both are used to prevent and treat motion sickness. 
It has been proved that anisodamine and scopolamine have equal anti-motion sickness effect. Moreover, anisodamine does not induce drowsiness, blurred vision, or other side effects, as does scopolamine. Therefore, according to study of these two agents, anisodamine is more suitable for anti-motion sickness than scopolamine. 
Accordingly, in our experiment, we selected anisodamine as an anti-motion sickness drug and investigated the effect of anisodamine on motion sickness and CGRP. Our results show that anisodamine administered orally before stimulation can alleviate the symptoms (i.e. CTA) of motion sickness (Figure1). Importantly, this study demonstrates for the first time that this medication can also significantly reduce the expression of CGRP in the vestibular efferent nucleus and the vestibular nucleus of rats that have undergone rotary stimulation (, ). This finding could be very helpful not only to further support a link between CGRP and motion sickness but also to motivate the use of CGRP as a potential biomarker for developing a specific test or new medication for motion sickness.