Stress-Related Alterations of Visceral Sensation: Animal Models for Irritable Bowel Syndrome Study.
- Author:
Muriel LARAUCHE
1
;
Agata MULAK
;
Yvette TACHE
Author Information
1. CURE/Digestive Diseases Research Center and Center for Neurobiology of Stress, Digestive Diseases Division, Department of Medicine, David Geffen School of Medicine, UCLA and VA Greater Los Angeles Healthcare System, Los Angeles, California, USA. mlarauche@mednet.ucla.edu
- Publication Type:Review
- Keywords:
Irritable bowel syndrome;
Models, animal;
Pain
- MeSH:
Animals;
Axis, Cervical Vertebra;
Irritable Bowel Syndrome;
Models, Animal;
Models, Theoretical;
Sprains and Strains;
Treatment Outcome;
Visceral Pain
- From:Journal of Neurogastroenterology and Motility
2011;17(3):213-234
- CountryRepublic of Korea
- Language:English
-
Abstract:
Stressors of different psychological, physical or immune origin play a critical role in the pathophysiology of irritable bowel syndrome participating in symptoms onset, clinical presentation as well as treatment outcome. Experimental stress models applying a variety of acute and chronic exteroceptive or interoceptive stressors have been developed to target different periods throughout the lifespan of animals to assess the vulnerability, the trigger and perpetuating factors determining stress influence on visceral sensitivity and interactions within the brain-gut axis. Recent evidence points towards adequate construct and face validity of experimental models developed with respect to animals' age, sex, strain differences and specific methodological aspects such as non-invasive monitoring of visceromotor response to colorectal distension as being essential in successful identification and evaluation of novel therapeutic targets aimed at reducing stress-related alterations in visceral sensitivity. Underlying mechanisms of stress-induced modulation of visceral pain involve a combination of peripheral, spinal and supraspinal sensitization based on the nature of the stressors and dysregulation of descending pathways that modulate nociceptive transmission or stress-related analgesic response.
