Identification of neural networks that contribute to motion sickness through principal components analysis of fos labeling induced by galvanic vestibular stimulation.
Motion sickness is a complex condition that includes both overt signs (e.g., vomiting) and more covert symptoms (e.g., anxiety and foreboding). The neural pathways that mediate these signs and symptoms are yet to identified. This study mapped the distribution of c-fos protein (Fos)-like immunoreactivity elicited during a galvanic vestibular stimulation paradigm that is known to induce motion sickness in felines. A principal components analysis was used to identify networks of neurons activated during this stimulus paradigm from functional correlations between Fos labeling in different nuclei. This analysis identified five principal components (neural networks) that accounted for greater than 95% of the variance in Fos labeling. Two of the components were correlated with the severity of motion sickness symptoms, and likely participated in generating the overt signs of the condition. One of these networks included neurons in locus coeruleus, medial, inferior and lateral vestibular nuclei, lateral nucleus tractus solitarius, medial parabrachial nucleus and periaqueductal gray. The second included neurons in the superior vestibular nucleus, precerebellar nuclei, periaqueductal gray, and parabrachial nuclei, with weaker associations of raphe nuclei. Three additional components (networks) were also identified that were not correlated with the severity of motion sickness symptoms. These networks likely mediated the covert aspects of motion sickness, such as affective components. The identification of five statistically independent component networks associated with the development of motion sickness provides an opportunity to consider, in network activation dimensions, the complex progression of signs and symptoms that are precipitated in provocative environments. Similar methodology can be used to parse the neural networks that mediate other complex responses to environmental stimuli.
Department of Otolaryngology, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America ; Department of Bioengineering, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America ; Department of Communication Sciences and Disorders, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America ; Department of Neurobiology, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.
Carey D
CD
Balaban
Department of Otolaryngology, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.
Sarah W
SW
Ogburn
Department of Otolaryngology, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.
Susan G
SG
Warshafsky
Department of Otolaryngology, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America ; Department of Neuroscience, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.
Abdul
A
Ahmed
Department of Otolaryngology, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America ; Department of Neuroscience, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.
Bill J
BJ
Yates
D000818:Animals; D002415:Cats; D004558:Electric Stimulation; D005260:Female; D008297:Male; D009041:Motion Sickness / Q000503:physiopathology*; D016571:Neural Networks, Computer; D025341:Principal Component Analysis; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism*; D014726:Vestibular Nuclei / Q000502:physiology*
D016760:Proto-Oncogene Proteins c-fos