Effect of an emetic gastrointestinal input on the processing of labyrinthine inputs by cerebellar rostral fastigial nucleus neurons (1130.7)

Abstract

Multiple inputs can elicit nausea and vomiting, including ingested toxins and vestibular signals. Amongst the nervous system regions believed to participate in generating motion sickness is the cerebellar rostral fastigial nucleus (rFN). In addition, there is evidence that gastrointestinal inputs are transmitted to rFN through a variety of pathways, including projections from the dorsal motor nucleus of the vagus and area postrema. These observations raise the hypothesis that GI inputs could change motion sickness susceptibility by altering the processing of labyrinthine inputs by rFN neurons. To test this hypothesis, we recorded activity from rFN neurons in decerebrate cats, and compared their responses to whole‐body rotations before and after the intragastric infusion of the emetic compound copper sulfate (CuSO4). Some (18%) rFN neurons had complex responses to vestibular stimulation, particularly responses to only one direction of rotation (known as STC behavior). Such complex responses would be expected in a brain area that participates in generating motion sickness. The spatial and temporal characteristics of these responses changed little after injection of CuSO4. Although infusion of CuSO4 affected gains of responses to rotations of ~25% rFN neurons, the effects were inconsistent (CuSO4 augmented responses in some cells and decremented responses in others). CuSO4 resulted in pronounced changes in responses to rotations of a significantly larger fraction (Chi‐squared test, p<0.05) of neurons in other brain regions that mediate nausea and vomiting, including the parabrachial nucleus and the “vomiting center” (caudal medullary lateral tegmental field). These data suggest that integration of vestibular and GI inputs by rFN neurons plays a limited role in affecting motion sickness susceptibility.Grant Funding Source: NIH grant R01‐DC03732