Concas A, Salis M, Biggio G
Life Sci. 1983 Mar 14;32(11):1175-82. doi: 10.1016/0024-3205(83)90185-6.
Rats were treated with repeated intraventricular injections of ethyl-beta-carboline-3-carboxylate (beta-CCE) (10 micrograms/rat, twice daily for 8 days), 36 h after the last injection, the total number of 3H-diazepam binding sites was increased in the cerebral cortex, cerebellum and hippocampus by 63, 51 and 38%, respectively. On the other hand, there were no significant differences in the dissociation constants (KD) between beta-CCE and solvent treated rats. In contrast, chronic beta-CCE administration failed to change the number of the apparent affinity of 3H-beta-CCE binding sites in all the brain areas examined. The results suggest that beta-CCE is an antagonist at the 3H-diazepam binding sites.
给大鼠反复脑室内注射β-咔啉-3-羧酸乙酯(β-CCE)(10微克/只,每日两次,共8天),末次注射36小时后,大脑皮层、小脑和海马中3H-地西泮结合位点总数分别增加了63%、51%和38%。另一方面,β-CCE处理组大鼠与溶剂处理组大鼠之间的解离常数(KD)无显著差异。相比之下,长期给予β-CCE未能改变所有检测脑区中3H-β-CCE结合位点的表观亲和力数量。结果表明,β-CCE是3H-地西泮结合位点的拮抗剂。