Sarnyai Z, Bíró E, Penke B, Telegdy G
Institute of Pathophysiology, Albert Szent-Györgyi Medical University, Szeged, Hungary.
Brain Res. 1992 Aug 28;589(1):154-6. doi: 10.1016/0006-8993(92)91176-f.
The role of endogenous corticotropin-releasing factor (CRF) in the cocaine-induced corticosterone response was investigated by using the immunoneutralization and receptor blockade of endogenous CRF. Pretreatment with different dilutions (1:5, 1:10 and 1:20, i.c.v.) of CRF antibody and different doses of an antagonist for CRF receptors, alpha-helical CRF9-41 (alpha h-CRF, 0.001-1.0 micrograms, i.c.v.), dose-dependently prevented the cocaine-induced increase in corticosterone level. These results support the hypothesis that the activation of the hypothalamo-pituitary-adrenal (HPA) axis by cocaine is mediated through the release of endogenous CRF.
通过对内源性促肾上腺皮质激素释放因子（CRF）进行免疫中和及受体阻断，研究了内源性CRF在可卡因诱导的皮质酮反应中的作用。用不同稀释度（脑室内注射，1:5、1:10和1:20）的CRF抗体以及不同剂量的CRF受体拮抗剂α-螺旋CRF9-41（αh-CRF，0.001 - 1.0微克，脑室内注射）进行预处理，可剂量依赖性地阻止可卡因诱导的皮质酮水平升高。这些结果支持以下假说：可卡因对下丘脑-垂体-肾上腺（HPA）轴的激活是通过内源性CRF的释放介导的。
