Overmier J B, Murison R, Ursin H, Skoglund E J
Behav Neurosci. 1987 Apr;101(2):246-53. doi: 10.1037//0735-7044.101.2.246.
Gastric ulceration in rats is exacerbated by allowing a so-called recovery period after exposure to an ulcerogenic stressor. One hypothesis, which has support from pharmacological studies, argues that this effect is brought about by a rebound of parasympathetic activation. We tested this parasympathetic rebound hypothesis by presenting animals with a fear-inducing (sympathetic-activating) conditioned stimulus (CS) after 2 hr of water-restraint stress. Contrary to the hypothesis, presentation of such a CS increased severity of ulceration compared with those animals that did not receive the CS after restraint stress and control animals. These ulceration data favor instead a sustained activation hypothesis for ulceration, whereby presentation of the CS effectively prolonged the length of time during which animals were under stress, thus enhancing the degree of ulceration. Measurement of plasma corticosterone however indicated a negative correlation between adrenocortical activity and degree of gastric ulceration, contrary to that expected by a sustained activation hypothesis. It is suggested that this inconsistency may be because of the activating of a pituitary-endorphinogenic mediated stress analgesia.
在暴露于致溃疡应激源后给予所谓的恢复期，会加剧大鼠的胃溃疡。一种有药理学研究支持的假说认为，这种效应是由副交感神经激活的反弹引起的。我们通过在水束缚应激2小时后向动物呈现诱发恐惧（激活交感神经）的条件刺激（CS）来检验这种副交感神经反弹假说。与该假说相反，与束缚应激后未接受CS的动物和对照动物相比，呈现这样的CS会增加溃疡的严重程度。这些溃疡数据反而支持溃疡的持续激活假说，即呈现CS有效地延长了动物处于应激状态的时间，从而增强了溃疡程度。然而，血浆皮质酮的测量表明肾上腺皮质活动与胃溃疡程度之间呈负相关，这与持续激活假说所预期的相反。有人认为，这种不一致可能是由于垂体 - 内啡肽介导的应激镇痛的激活。
