Gomar M D, Fernández B, Castillo J L, del Aguila C M, Acuña-Castroviejo D
Departamento de Fisiologia, Facultad de Medicina, Universidad de Granada, Spain.
Neuroreport. 1993 Dec 13;5(3):252-4. doi: 10.1097/00001756-199312000-00017.
Seven-day hypophysectomized rats were intracerebroventricularly (i.c.v.) injected with beta-endorphin, ACTH1-10 or beta-endorphin+ACTH1-10 (10-20 ng of each compound) and the [3H]flunitrazepam ([3H])FNZ) binding to the rat cerebral cortex of hypophysectomized rats was assayed one hour later. The i.c.v. injection of ACTH1-10 (10-20 ng) or beta-endorphin (10-20 ng) significantly increased [3H]FNZ binding to a similar extent. The effect of i.c.v. injection of ACTH1-10 on brain binding was blunted by simultaneous beta-endorphin administration at the same doses. The i.c.v. naloxone injection (10-20 ng) did not modify the effect of ACTH1-10 (10 ng) on [3H]FNZ binding, but counteracted, in a dose-related manner, the blocking effect of beta-endorphin on ACTH1-10-dependent brain [3H]FNZ binding. The results suggest the existence of an opioid-melanopeptide integration to control brain benzodiazepine receptors.
对垂体切除7天的大鼠进行脑室内(i.c.v.)注射β-内啡肽、促肾上腺皮质激素1-10(ACTH1-10)或β-内啡肽+ACTH1-10(每种化合物10-20纳克),1小时后测定垂体切除大鼠大脑皮质中[3H]氟硝西泮([3H]FNZ)的结合情况。脑室内注射ACTH1-10(10-20纳克)或β-内啡肽(10-20纳克)能显著增加[3H]FNZ结合,且程度相似。同时注射相同剂量的β-内啡肽会减弱脑室内注射ACTH1-10对大脑结合的影响。脑室内注射纳洛酮(10-20纳克)不会改变ACTH1-10(10纳克)对[3H]FNZ结合的作用,但会以剂量相关的方式抵消β-内啡肽对ACTH1-10依赖的大脑[3H]FNZ结合的阻断作用。结果表明存在一种阿片-促黑素细胞激素整合机制来控制大脑苯二氮䓬受体。