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Evidences of submucosal neuronal plasticity in distal colon of chronic restraint stress rat
Author(s) -
Poonyachoti Sutthasinee,
Deachapunya Chatsri
Publication year - 2007
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.21.6.a1319-d
Subject(s) - reflex , medicine , endocrinology , damgo , chronic stress , ussing chamber , substance p , pathogenesis , receptor , opioid , neuropeptide , opioid receptor , secretion
Chronic stress is involved in the pathogenesis of gastrointestinal disorders. The phenotype and function of neurons in submucosal reflex may be subjects for this evidence. We investigated whether enteric neuronal reflex was changed during chronic stress. Male Wistar rats were immobilized for 14 days (1‐hr/day). Distal colonic epithelium was isolated to measure Isc and Rt by Ussing chamber techniques. Isc and Rt of stressed‐rat colonic segments were lower than those in control rats. The secretory effects of vanilloid capsaicin (3 μM) mediated by VR‐1 on sensory neurons was decreased by 70% in stressed‐rat colon. Basolateral addition of DAMGO, DSLET or U‐50,488 (1 μM), μ‐, δ‐ or μ‐opioid receptor (OR) agonists respectively, diminished the basal Isc of control rat colon by 20–30%, whereas only U‐50,488 decreased the baseline Isc of stress rat colon by 20%. Substance P (SP, 1 μM) produced the same magnitude of Isc response in both control and stress rat colon. Pretreatment with DAMGO potentiated the SP response by 2‐fold in stress rats. These findings suggested that the submucosal neuronal reflex mediated through VR‐1 and opioid receptors was modified in distal colon of chronic stress rat. The changes in submucosal neuronal plasticity may be the cause of stress induced gastrointestinal disorders. This work was supported by the Thailand Research Fund (RSA 4780010) and Chulalongkorn University.