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.