title: Anti-stress effects of transcutaneous electrical nerve stimulation (TENS) on colonic motility in rats.
abstract: BACKGROUND
  Disorders of colonic motility may contribute to symptoms in patients with irritable bowel syndrome (IBS), and stress is widely believed to play a major role in developing IBS. Stress increases corticotropin releasing factor (CRF) of the hypothalamus, resulting in acceleration of colonic transit in rodents. In contrast, hypothalamic oxytocin (OXT) has an anti-stress effect via inhibiting CRF expression and hypothalamic-pituitary-adrenal axis activity. Although transcutaneous electrical nerve stimulation (TENS) and acupuncture have been shown to have anti-stress effects, the mechanism of the beneficial effects remains unknown.
  
  
  OBJECTIVE
  We tested the hypothesis that TENS upregulates hypothalamic OXT expression resulting in reduced CRF expression and restoration of colonic dysmotility in response to chronic stress.
  
  
  METHODS
  Male SD rats received different types of stressors for seven consecutive days (chronic heterotypic stress). TENS was applied to the bilateral hind limbs every other day before stress loading. Another group of rats did not receive TENS treatment.
  
  
  RESULTS
  TENS significantly attenuated accelerated colonic transit induced by chronic heterotypic stress, which was antagonized by a central injection of an OXT antagonist. Immunohistochemical study showed that TENS increased OXT expression and decreased CRF expression at the paraventricular nucleus (PVN) following chronic heterotypic stress.
  
  
  CONCLUSIONS
  It is suggested that TENS upregulates hypothalamic OXT expression which acts as an anti-stressor agent and mediates restored colonic dysmotility following chronic stress. TENS may be useful to treat gastrointestinal symptoms associated with stress.
authors.affiliation: Department of Surgery, Zablocki VA Medical Center, Medical College of Wisconsin, 5000 West National Avenue, Milwaukee, WI 53295, USA.
authors.forename: Sazu
authors.initials: S
authors.lastname: Yoshimoto
authors.forename: Reji
authors.initials: R
authors.lastname: Babygirija
authors.forename: Anthony
authors.initials: A
authors.lastname: Dobner
authors.forename: Kirk
authors.initials: K
authors.lastname: Ludwig
authors.forename: Toku
authors.initials: T
authors.lastname: Takahashi
mesh_terms: D000818:Animals; D002908:Chronic Disease; D003106:Colon / Q000503:physiopathology*; D003346:Corticotropin-Releasing Hormone / Q000037:antagonists & inhibitors / Q000378:metabolism; D004195:Disease Models, Animal; D025461:Feedback, Physiological; D005769:Gastrointestinal Motility; D007030:Hypothalamo-Hypophyseal System / Q000378:metabolism / Q000503:physiopathology; D043183:Irritable Bowel Syndrome / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy; D008297:Male; D010121:Oxytocin / Q000378:metabolism; D010913:Pituitary-Adrenal System / Q000378:metabolism / Q000503:physiopathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013315:Stress, Psychological / Q000150:complications / Q000378:metabolism / Q000503:physiopathology; D004561:Transcutaneous Electric Nerve Stimulation / Q000379:methods*; D016896:Treatment Outcome
chemical_list: D010121:Oxytocin; D003346:Corticotropin-Releasing Hormone