| Popis: |
Passive motion can induce kinetosis (motion sickness, MS) in susceptible individuals. MS is an evolutionary conserved mechanism caused by mismatches between motion-related sensory information and past visual and motion memory, triggering a malaise accompanied by hypolocomotion, hypothermia, hypophagia and aversion to novel foods presented coincidentally. Vestibular nuclei (VN) are critical for the processing of movement input, and motion-induced activation of VN neurons recapitulates MS-related signs. However, the genetic identity of VN neurons mediating MS-related autonomic and aversive responses remains unknown. Here, we identify a glutamatergic vestibular circuitry necessary to elicit MS-related behavioral responses, defining a central role of cholecystokinin (CCK)- expressing glutamatergic VN neurons in vestibular-induced malaise. Moreover, we show that CCK VN inputs onto the parabrachial nucleus activate Calca-expressing neurons and are sufficient to establish hypothermia and aversion to novel food. Together, we provide novel insight into the neurobiological regulation of MS, unravelling key genetically defined neural substrates for kinetosis. |
