title: Conditioned emotional response in rats enhances colonic motility through the central release of corticotropin-releasing factor.
abstract: The effect of a mental stress model corresponding to conditioned fear on cecocolonic motility was evaluated electromyographically in intact and hypophysectomized rats equipped with electrodes implanted in the cecum and proximal colon over a long period and a small polyethylene catheter inserted into the right lateral ventricle of the brain. Intact fasted and fed rats showed an increase of 82.3% and 67.2%, respectively, in colonic spike-burst frequency when placed for 30 minutes in a box in which they had previously received electrical shocks in their feet. Intracerebroventricular administration of corticotropin-releasing factor (0.5 micrograms/kg) mimicked the effects of mental stress and increased cecocolonic spike-burst frequency by 75.8%. The specific corticotropin-releasing factor receptor antagonist alpha-helical CRF9-41 given intracerebroventricularly (5 micrograms/kg) prevented both the effects of mental stress and corticotropin-releasing factor (0.5 micrograms/kg intracerebroventricularly) on colonic spike-burst frequency. In contrast, diazepam (0.5 mg/kg IM) suppressed colonic hypermotility induced by mental stress but not that resulting from intracerebroventricular injection of corticotropin-releasing factor (0.5 micrograms/kg). Increased colonic spike-burst frequency induced either by stress or by central administration of corticotropin-releasing factor was not prevented by hypophysectomy. It was concluded that mental stress increases the frequency of cecocolonic spike-burst activity and that these effects are related to the central release of corticotropin-releasing factor because they are blocked by a corticotropin-releasing factor antagonist and reproduced by intracerebroventricular administration of corticotropin-releasing factor. Moreover, mental stress-induced colonic motor alterations are mediated by the autonomic nervous system rather than by the hypothalamopituitary axis because they are not abolished by hypophysectomy.
authors.affiliation: Department of Pharmacology, Institute National de la Recherche Agronomique, Toulouse, France.
authors.forename: M
authors.initials: M
authors.lastname: Gue
authors.forename: J L
authors.initials: JL
authors.lastname: Junien
authors.forename: L
authors.initials: L
authors.lastname: Bueno
mesh_terms: D000818:Animals; D001921:Brain / Q000378:metabolism*; D003213:Conditioning, Psychological; D003346:Corticotropin-Releasing Hormone / Q000037:antagonists & inhibitors / Q000378:metabolism* / Q000494:pharmacology; D005239:Fear / Q000502:physiology; D005769:Gastrointestinal Motility / Q000187:drug effects / Q000502:physiology*; D007016:Hypophysectomy; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology; D008297:Male; D010446:Peptide Fragments / Q000494:pharmacology; D010913:Pituitary-Adrenal System / Q000503:physiopathology; D051381:Rats; D013315:Stress, Psychological / Q000503:physiopathology*
chemical_list: D010446:Peptide Fragments; D003346:Corticotropin-Releasing Hormone; C045089:corticotropin releasing hormone (9-41)