Vestibular CCK signaling drives motion sickness-like behavior in mice

Pablo Machuca-Márquez, Laura Sánchez-Benito, Fabien Menardy, Andrea Urpi, Mònica Girona, Emma Puighermanal, Isabella Appiah, Richard D. Palmiter, Elisenda Sanz, Albert Quintana

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Resumen

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.
Idioma originalInglés
Número de artículoe2304933120
Páginas (desde-hasta)e2304933120
Número de páginas11
PublicaciónProceedings of the National Academy of Sciences of the United States of America
Volumen120
N.º44
DOI
EstadoPublicada - 17 oct 2023

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