晕动症易感性存在显著的个体差异，但相关分子机制尚不清楚。我们发现人群晕动症易感性与嗅觉受体Olr8(人同源性受体OR52J3)胞内段C端rs57026471位点基因多态性相关；通过蛋白组学实验发现OR52J3受体胞内段C端多肽与前庭核内酪蛋白激酶2（CK2）α和β亚单位具有较强相互作用，并在前庭核共表达；已知，CK2可通过磷酸化作用影响谷氨酸NMDA受体及胆碱能M3受体膜表达及活性，亦可调节组蛋白磷酸化及乙酰化过程，影响基因表达，以提高机体对特殊环境的耐受力；本研究拟观察CK2与Olr81及其突变体结合活性的差异，及对前庭核神经元NMDA及M3受体膜表达及活性的影响；探索CK2-Olr81相互作用对新生及成年大鼠反复加速度暴露后，前庭核神经元表观遗传变化特征及所调控的相关基因表达的影响，以期阐明CK2-Olr81相互作用影响晕动症易感性的分子机制，为提高易感人群晕动症耐受能力提供新途径。

The individual difference of motion sickness susceptibility is great, but the related molecular mechanism is still unclear. We found that motion sickness susceptibility in humans is associated with the single nucleotide polymorphism of rs57026471 in C terminal of intracellular region of OR52J3-the human homology of olfactory receptor Olr81 in rat. Our proteomics study revealed that C terminal of intracellular region of OR52J3 significantly interacts with α and β subunit of casein kinase 2 (CK2) and co-expresses with each other in the vestibular nucleus. It is known that CK2 can affect the memebrane surfacing and activity of glutamatergic NMDA receptor and cholinergic M3 receptor via phosphorylation regulation. It also can regulate the process of phosphorylation and acetylation of histones, affect gene expression and subsequently enhance the endurance to special environment. In this project, we will observe the difference in the interaction between CK2 and Olr81 or its mutants and its effects on memebrane surfacing and activity of NMDA and M3 receptor. We also try to explore the effect of CK2-Olr81 interaction on epigenetics character and related gene expression profile in vestibular nucleus neurons in newborn and adult rats exposed to acceleration repeatedly. The purpose of these experiments is to clarify molecular mechanism underlying the involvement of CK2-Olr81 interaction in motion sickness susceptibility and provide a novel way to enhance motion sickness endurance in susceptible subjects.