Abstract
Motion sickness (MS) is an acute disorder that occurs in healthy individuals worldwide regardless of gender, age, or ethnicity. Our study used a mouse model to rule out the effects of any psychological factors related to MS and EA. Subjects were randomly separated into four groups, namely the control group (Con), motion sickness inducing group (MS), mentioning sickness inducing with electroacupuncture treatment group (EA) and motion sickness inducing only in TRPV1 knockout mice group (TRPV1−/−). The consumption of kaolin, a non-nutrient substance, was measured as a behavior observed response of an emetic reflex in a murine model. This behavior is referred to as pica behavior. Our results showed that pica behavior was observed in the MS group. Moreover, kaolin consumption in the EA group decreased to the average baseline of the control group. A similar result was observed in TRPV1 null mice. We also observed an increase of TRPV1 and related molecules in the thalamus, hypothalamic and brain stem after MS stimulation and a significant decrease in the EA and TRPV1 null groups. This is the first study to demonstrate that TRPV1 pathways are possibly associated with mechanisms of MS, and can be attended through EA or TRPV1 genetic manipulation.
Highlights
Motion sickness (MS) occurs in healthy individuals worldwide regardless of gender, age, or ethnicity
Throughout the experimental period, we observed a significantly increased kaolin consumption in the MS group (Fig. 1A; 1.13 ± 0.19, p < 0.05) compared with that in the control group
We showed that pERK levels were significantly increased in the thalamus after MS induction (Fig. 5B), whereas this increase was attenuated in the electroacupuncture treatment group (EA) and TRPV1−/− groups (Fig. 5C and D)
Summary
Motion sickness (MS) occurs in healthy individuals worldwide regardless of gender, age, or ethnicity. The input signals from vestibular organs in the inner ear and somatosensory cascade to the thalamus, the center of sensory information, before flowing to other parts of the brain, which associate with MS responses, including the hypothalamic and brain stem regions. The oculomotor system signal pathway initiates in the brain stem, and cooperates with the vestibular system for positional recognition responses. The mismatch signals from these three brain areas are important in the exploration of the TRPV1 expression in MS in mice. Many reports have described the distribution of TRPV1 in widely expressed brain areas, including the thalamus, hypothalamus, hippocampus, amygdala, cerebellum, and dorsal root ganglia[17,19,20]. Intracellular signals cascade to proteins, including protein kinases, mitogen-activated protein kinase (MAPK), and cyclic AMP-response element binding protein (CREB). Some aspects of MAPK signaling associate with the calcium/calmodulin-dependent protein kinase and CREB in neuronal pathways[24]
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