A dual action of stress on pain modulation has been well characterized in the somatic pain studies, while much less is known in the visceral field. In the context of clinical observations that stress plays a critical role in the pathophysiology, symptoms presentation and clinical outcome of functional gastrointestinal disorders such as irritable bowel syndrome (IBS), a number of acute and chronic stress models have been developed in rodents. Recent data have demonstrated that the state of the animal tested (naïve vs. exposed to surgery), its social environment (group housing vs. single housing), the methods used to record visceromotor responses (EMG requiring surgery and antibiotic after surgery vs. manometry not requiring surgery/antibiotic) can significantly affect the analgesic response to exteroceptive stressors. Growing body of evidence indicates that a new noninvasive solid-state manometric method to monitor viscero motor response is valuable to unravel both analgesia and hyperalgesia without confounding factors. This is of critical importance regarding the recently recognized role of a compromised engagement of the inhibitory descending pain pathways in IBS patients. Better understanding of mechanisms of stress-related modulation of visceral pain leading to analgesia and hyperalgesia, along with the role of sex-dependent factors and complex interactions of the brain-gut-enteric microbiota axis may lead to new therapeutic targets in IBS.
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