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Conditioned emotional response in rats enhances colonic motility through the central release of corticotropin-releasing factor

1991; Elsevier BV; Volume: 100; Issue: 4 Linguagem: Inglês

10.1016/0016-5085(91)90270-u

1528-0012

M. Gué, J.L. Junien, Lionel Bueno,

Neuroendocrine regulation and behavior

The effect of a mental stress model corresponding to conditioned fear on cecocolonic motility was evaluated electromyographically in intact and hypophy sectomized 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 Fg/kg) mimicked the effects of mental stress and increased cecocolonic spikeburst frequency by 75.8%.The specific corticotropinreleasing factor receptor antagonist o-helical CRF,,, given intracerebroventricularly (5 pg/kg) prevented both the effects of mental stress and corticotropinreleasing factor (0.5 p.g/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 ug/kg).Increased colonic spike-burst frequency induced either by stress or by central administration of corticotropinreleasing 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.