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Environmental Enrichment Reverses Chronic Stress‐Induced Brain‐Gut Axis Dysfunction
Author(s) -
Love James,
Johnson Anthony,
Ligon Casey,
Meerveld Beverley GreenwoodVan
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.921.1
Subject(s) - irritable bowel syndrome , visceral pain , medicine , distension , hyperalgesia , endocrinology , analysis of variance , somatic cell , anesthesia , nociception , chemistry , receptor , biochemistry , gene
Stress‐induced visceral hyperalgesia is a contributing factor in irritable bowel syndrome (IBS), a highly prevalent brain‐gut disorder characterized by chronic visceral pain. Previously we showed that repetitive daily exposure to a water avoidance stressor (WAS) for 1 hr/day for 7 days induced visceral and somatic hyperalgesia in a rodent model. A positive environment enrichment (EE) is known to have a critical role in brain development and stress reactivity, however it is unknown whether EE is capable of reversing stress‐induced viscero‐somatic hypersensitivity. Methods Experiments were performed on male F344 rats that were housed in either standard housing (SH) or in large cages filled with toys and food treats for EE. The effect of EE (7–14 days) before and/or during the WAS or sham stress (SHAM) induced visceral and somatic hypersensitivity was investigated (n=4/group). Visceral sensitivity was assessed via a visceromotor response (VMR) to graded pressure (0–60 mmHg) of isobaric colorectal distension (CRD). Somatic sensitivity was measured via von Frey filaments applied to the hind paw. Results were analyzed with one‐ or two‐way ANOVA with a Bonferroni's correction. Results Compared to male rats placed in SH, we found that EE for 14 days before and during the 7 days of WAS produced a significant attenuation in visceral ( 60 mmHg, WAS+EE=19.8±4.0 vs. WAS+SH=28.5±4.1 abdominal contractions, p<0.05) and somatic hypersensitivity (WAS+EE=85.7±7.4 vs. WAS+SH=65.6±4.5 g withdrawal threshold, p<0.01). In a similar fashion, rats housed with EE for only 7 days before and during the WAS procedure also demonstrated a significant reduction in visceral hypersensitivity and somatic allodynia. However, when rats were not pre‐exposed to EE and only housed in an EE during the time of the WAS procedure, there was no significant inhibition of WAS‐induced visceral hypersensitivity ( 60mmHg, WAS+EE=27.7±11.0 abdominal contractions) or somatic allodynia (WAS+EE=59.3±5.1 g). Summary and Conclusions Our data reveal that pre‐exposure of adult animals to short‐term EE prevents visceral and somatic hypersensitivity induced by chronic repetitive stress. Future experiments are designed to understand the basic underlying molecular mechanisms responsible for the positive effects of EE on stress‐induced visceral and somatic hyperalgesia and its implications in the treatment of brain‐gut axis dysfunction. Support or Funding Information Dr. Greenwood‐Van Meerveld would like to acknowledge the funding provided by her Department of Veterans Affairs Merit Grant – I01BX002188. Dr. Greenwood‐Van Meerveld is the recipient of a Senior Research Career Scientist award (1IK6BX003610) from the Department of Veterans Affairs. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .