Gue M, Junien J L, Bueno L
Department of Pharmacology, Institute National de la Recherche Agronomique, Toulouse, France.
Gastroenterology. 1991 Apr;100(4):964-70. doi: 10.1016/0016-5085(91)90270-u.
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.
在长期植入电极于盲肠和近端结肠且在脑右侧脑室插入一根小聚乙烯导管的完整大鼠和垂体切除大鼠中，通过肌电图评估了对应条件性恐惧的精神应激模型对盲结肠运动的影响。完整的禁食和进食大鼠，当被置于一个它们先前足部曾接受电击的盒子中30分钟时，结肠棘波爆发频率分别增加了82.3%和67.2%。脑室内注射促肾上腺皮质激素释放因子（0.5微克/千克）模拟了精神应激的作用，使盲结肠棘波爆发频率增加了75.8%。脑室内给予特异性促肾上腺皮质激素释放因子受体拮抗剂α - 螺旋CRF9 - 41（5微克/千克）可预防精神应激和促肾上腺皮质激素释放因子（脑室内注射0.5微克/千克）对结肠棘波爆发频率的影响。相比之下，地西泮（0.5毫克/千克，肌肉注射）抑制了精神应激诱导的结肠运动亢进，但不抑制脑室内注射促肾上腺皮质激素释放因子（0.5微克/千克）所导致的结肠运动亢进。垂体切除并不能预防由应激或中枢给予促肾上腺皮质激素释放因子所诱导的结肠棘波爆发频率增加。得出的结论是精神应激增加了盲结肠棘波爆发活动的频率，并且这些作用与促肾上腺皮质激素释放因子的中枢释放有关，因为它们被促肾上腺皮质激素释放因子拮抗剂所阻断，并可通过脑室内给予促肾上腺皮质激素释放因子而重现。此外，精神应激诱导的结肠运动改变是由自主神经系统介导而非下丘脑 - 垂体轴介导，因为垂体切除并不能消除这些改变。
