In this study, vestibular caloric stimulation (CS) inhibited noradrenergic (NA) neurons of the locus coeruleus (LC) in rats. The vestibular input can be modified by the ventrolateral medulla (VLM), which then inhibits the LC neuronal activity via GABAA receptors. Clinically, CS induces vertigo in humans. Thus, LC-NA inhibition may be involved in the development of vertigo. Moreover, it is speculated that Sopite syndrome, one of the major symptom complexes of motion sickness, is also evoked by LC-NA inhibition. The central LC-NA neuronal system may participate in vertigo and motion sickness independent of the histaminergic neuronal system. In contrast, the cholinergic neuronal system may mediate LC-NA inhibition during the vestibulo-atonomic reflex. The LC-NA system projects to most higher centers and affects sensory information processing. Therefore, it is suggested that the suppression of sensory information processing induced by LC-NA inhibition causes drowsiness, one of the major symptoms of vertigo and motion sickness. It is also speculated that LC-NA inhibition participates in the development of sensory mismatch during vertigo and motion sickness.