FIG 7.

Proposed model for rotavirus gut motility and gut-brain cross talk. Sensory information from the gut is relayed from afferent vagal nerves to the CNS, which keeps the autonomic nervous system in balance (left). During infection (right), rotavirus can cause excessive release of serotonin (green dots) from enterochromaffin cells and thereby cause activation of afferent nerves (1), which are relayed through the nodose ganglion in the spinal cord or directly reach the CNS to modulate discrete regions, including the BNST and NTS (2). In the CNS, the signal is processed, and the responses project in efferent sympathetic nerves to the gut. Reduced release of noradrenaline (NA) from sympathetic nerves (3) will reduce the “brake” (4) and thus increase gut motility.