Abstract
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.
Highlights
Vomiting is usually considered to be a protective reflex to rid the body of ingested toxins
Three other animals (C62, C64, C02) exhibited overt behaviors indicating that the vestibular system was activated by the stimulus, sinusoidal head roll at the frequency of the stimulus, only one or two potential indicators of motion sickness were evident for each animal
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
Summary
Vomiting is usually considered to be a protective reflex to rid the body of ingested toxins. This response is elicited following surgery or exposure to radiation, during cancer chemotherapy or pregnancy, and even as a consequence of some psychological stimuli [1,2]. Many animals, including the most commonly used species in biomedical research (rodents and rabbits), lack the capacity to vomit [16]. This is due both to reduced muscularity of the diaphragm and a stomach geometry that is not well structured for moving contents towards the esophagus in non-emetic animals. The brainstem circuitry that regulates the respiratory muscle contractions that result in vomiting differs between emetic and non-emetic animals [16,17]
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