In the present study, we first proved that the bilateral microinjection of AVP into vestibular nuclei, similar to a rotatory stimulus, induced conditioned taste aversion in rats and that the application of SSR149415, an antagonist of AVP V1bR, blunted this CTA-inducing effect of AVP and rotatory stimulus-induced CTA, suggesting that AVP, through its action on the VN, could contribute to the development of motion sickness in rats via the mediation of V1bR. This evidence concerns the gene AVP and motion sickness.