Targeting TRPV1 to relieve motion sickness symptoms in mice by electroacupuncture and gene deletion

Sci Rep. 2018 Jul 9;8(1):10365. doi: 10.1038/s41598-018-23793-6.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Brain Stem / metabolism
  • Disease Models, Animal
  • Electroacupuncture*
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Gene Deletion
  • Hypothalamus / metabolism
  • Kaolin / administration & dosage
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Motion Sickness / genetics
  • Motion Sickness / pathology*
  • Motion Sickness / therapy
  • NF-kappa B / metabolism
  • Signal Transduction / genetics
  • TRPV Cation Channels / deficiency
  • TRPV Cation Channels / genetics*
  • TRPV Cation Channels / metabolism
  • Thalamus / metabolism

Substances

  • NF-kappa B
  • TRPV Cation Channels
  • TRPV1 protein, mouse
  • Kaolin
  • Extracellular Signal-Regulated MAP Kinases