| First Author | Machuca-Márquez P | Year | 2023 |
| Journal | Proc Natl Acad Sci U S A | Volume | 120 |
| Issue | 44 | Pages | e2304933120 |
| PubMed ID | 37847729 | Mgi Jnum | J:352887 |
| Mgi Id | MGI:7546754 | Doi | 10.1073/pnas.2304933120 |
| Citation | Machuca-Marquez P, et al. (2023) Vestibular CCK signaling drives motion sickness-like behavior in mice. Proc Natl Acad Sci U S A 120(44):e2304933120 |
| abstractText | Travel can induce 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 nausea. Vestibular nuclei (VN) are critical for the processing of movement input from the inner ear. 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 central role of cholecystokinin (CCK)-expressing VN neurons in motion-induced malaise. Moreover, we show that CCK VN inputs onto the parabrachial nucleus activate Calca-expressing neurons and are sufficient to establish avoidance to novel food, which is prevented by CCK-A receptor antagonism. These observations provide greater insight into the neurobiological regulation of MS by identifying the neural substrates of MS and providing potential targets for treatment. |
