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Differential Gene Expression Profile in the Rat Caudal Vestibular Nucleus is Associated with Individual Differences

Jun-Qin Wang1, Rui-Rui Qi1, Wei Zhou1

  • 1Department of Nautical Injury Prevention, Faculty of Navy Medicine, Second Military Medical University, Shanghai, China.

Plos One
|April 25, 2015
PubMed
Abstract

Insights

Motion sickness susceptibility in rats is linked to gene expression changes in the caudal vestibular nucleus. Targeting specific receptors like nicotinic cholinergic receptor alpha3 subunit and tachykinin neurokinin-1 receptor may offer therapeutic strategies.

Area of Science:

  • Neuroscience
  • Genetics

Background:

  • Individual differences in motion sickness (MS) susceptibility are significant.
  • The caudal vestibular nucleus (CVN) plays a crucial role in processing motion stimuli.
  • Understanding the molecular basis of MS susceptibility is essential for developing effective treatments.

Purpose of the Study:

  • To identify genes differentially expressed in the rat CVN associated with motion sickness susceptibility.
  • To investigate the functional role of these genes in motion sickness behavior and physiological responses.

Main Methods:

  • Rats were classified as motion sickness susceptible (MSS) or insusceptible (inMSS) based on behavioral responses to rotation.
  • Microarray analysis was performed on CVN tissue to identify differentially expressed genes.
  • Quantitative real-time PCR (RT-qPCR) was used to validate gene expression findings.
  • Pharmacological and genetic manipulations targeting candidate genes were conducted in the CVN.

Main Results:

  • 304 transcripts were differentially expressed between MSS and inMSS rats.
  • Key candidate genes identified include nicotinic cholinergic receptor (nAchR) α3 subunit, 5-hydroxytryptamine receptor 4 (5-HT4R), and tachykinin neurokinin-1 (NK1R).
  • Administration of an nAchR antagonist (mecamylamine) reduced MS symptoms and plasma β-endorphin levels in MSS rats.
  • NK1R antagonist and Olfactory Receptor 81 (Olr81) knockdown affected defecation responses, while 5-HT4R antagonist and Shc1 overexpression had no significant effect.

Conclusions:

  • Variations in CVN gene expression after motion stimulation contribute to individual differences in MS susceptibility.
  • Specific genes, such as nAchR α3 and NK1R, are potential therapeutic targets for motion sickness.
  • These findings provide a molecular basis for understanding MS variability and developing novel treatment strategies.

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