Biró E, Sarnyai Z, Penke B, Szabó G, Telegdy G
Department of Pathophysiology, Albert Szent-Györgyi Medical University, Szeged, Hungary.
Neuroendocrinology. 1993;57(2):340-5. doi: 10.1159/000126377.
The possible involvement of endogenous corticotropin-releasing factor (CRF) in the anxiogenic and pituitary-adrenal-axis-activating effects of cholecystokinin octapeptide sulfate ester (CCK 8) was investigated in rats. Intracerebroventricularly (i.c.v.) administered CCK 8 induced an anxiogenic response in an elevated plus-maze test, and enhanced the plasma corticosterone level. Pretreatment with different dilutions (1:10, 1:20 and 1:100, i.c.v.) of CRF antiserum and different doses of a CRF receptor antagonist, alpha-helical CRF (ahCRF, 0.001-1.0 microgram, i.c.v.) prevented the anxiogenic response to CCK 8 in a dose-dependent manner. None of the doses of CRF antiserum or ahCRF alone produced any alteration in either the elevated plus-maze paradigm or corticosterone level in saline-treated control rats. The results strongly suggest that the anxiogenic and hypothalamo-pituitary-adrenal-activating effects of CCK 8 are mediated via CRF.
在大鼠中研究了内源性促肾上腺皮质激素释放因子（CRF）可能参与硫酸八肽胆囊收缩素（CCK 8）的致焦虑和激活垂体-肾上腺轴的作用。脑室内（i.c.v.）注射CCK 8在高架十字迷宫试验中诱导出致焦虑反应，并提高了血浆皮质酮水平。用不同稀释度（1:10、1:20和1:100，i.c.v.）的CRF抗血清和不同剂量的CRF受体拮抗剂α-螺旋CRF（ahCRF，0.001 - 1.0微克，i.c.v.）进行预处理，以剂量依赖的方式预防了对CCK 8的致焦虑反应。单独使用任何剂量的CRF抗血清或ahCRF均未对生理盐水处理的对照大鼠的高架十字迷宫范式或皮质酮水平产生任何改变。结果强烈表明，CCK 8的致焦虑和下丘脑-垂体-肾上腺激活作用是通过CRF介导的。
