Nausea elicited by chemo- and radiotherapy, surgical intervention with anaesthesia, motion, and during pregnancy, is a major clinical problem as it is often resistant to anti-emetic drugs1. In contrast to the well-defined pathways mediating vomiting, the neural circuitry responsible for nausea is poorly understood, largely due to the lack of adequate indices of nausea in preclinical studies. Most mechanistic studies on nausea in humans come from perturbing vestibular or visual stimulation. The resulting cardinal symptoms of motion sickness are cold sweating, nausea and vomiting, and facial pallor; a few studies also report motion sickness-related hypothermia2 from cutaneous vasodilation in the limbs3. The aim of the present studies, therefore, was to investigate if similar motion-induced responses are present in rats and in house musk shrews (Suncus murinus – an insectivore possessing vomiting reflex). Under isoflurane anesthesia (2% in O2), adult male Wistar rats were implanted with telemetric transmitters to record core body temperature. One week later, the animals were administered 5-HT3 receptor antagonist ondansetron (0.5 mg/kg s.c.) or vehicle, and 30 min later were subjected to provocative motion (rotation 0.5 Hz, 40 min) in their home cages; the experiment was repeated one week later using a crossover design (n=7). The rotational stimulus provoked mild hypothermia (from 37.4±0.1 to 35.6±0.2°C, p<0.001) that was attenuated by ondansetron by 28% (P<0.05). In another groups of rats (un-instrumented, n=6) we used infrared thermography and found that rotation induced a transient increase of tail temperature (from 22.9±0.6 to 25.1±0.6°C p<0.05) indicative of vasodilation; this rise appeared to precede the fall in the core body temperature seen in the telemetered studies. Infrared thermography was also used to investigate skin temperature changes induced by motion (linear shaker, 1 Hz, 15 min) in S. murinus (n=6). All animals exhibited episodes of retching and/or vomiting (latency = 205±38 s) that was preceded by a transient increase in tail temperature (from 24.0±1.5 to 27.0±2.2°C, p<0.05). A fall of interscapular temperature (from 38.4±0.5 to 36.6±0.4°C, p<0.001) was also seen during motion testing. In conclusion, provocative motion appears to induce hypothermia via mechanisms presumably involving dilatation of the vascular bed of the tail. The tail vasodilation that precedes retching/vomiting in S. murinus, and the tail vasodilation in rats could form the basis of a potential index of nausea in experimental animals. The poor effect of ondansetron was predicted since it does not prevent motion sickness-induced nausea in man.