Bralet J, Lallemant A M
Arch Int Pharmacodyn Ther. 1975 Oct;217(2):332-41.
The influence of cocaine (10 mg/kg, i.m.) on the synthesis and the release of noradrenaline (NA) has been studied in rat brain. Cocaine pretreatment reduced significantly the amount of NA-3H synthetized from tyrosine-3H (TY-3H) in the whole brain and various cerebral structures. The synthesis rates of NA (estimated by calculation of the ratio: amount of NA-3H/tissular specific activity of TY-3H) were reduced by 40% in the whole brain, 30 and 60 min after administration of TY-3H. The rise of the NA endogenous level 10 min after administration of a monamine oxidase inhibitor (ranylcypromine) was inhibited after cocaine treatment. The release of NA has been studied after inhibition of its synthesis by alpha-methyl-paratyrosine. Cocaine pretreatment significantly delayed the disappearance rate of cerebral NA. The possible mechanisms by which cocaine reduced NA turnover are discussed.
研究了可卡因（10毫克/千克，肌肉注射）对大鼠脑内去甲肾上腺素（NA）合成及释放的影响。可卡因预处理显著降低了全脑及各种脑结构中由酪氨酸-3H（TY-3H）合成的NA-3H的量。给予TY-3H后30和60分钟，全脑中NA的合成率（通过计算NA-3H量与TY-3H组织比活性的比值估算）降低了40%。给予单胺氧化酶抑制剂（雷尼替丁）10分钟后，NA内源性水平的升高在可卡因处理后受到抑制。在用α-甲基对酪氨酸抑制NA合成后，研究了NA的释放。可卡因预处理显著延迟了脑内NA的消失速率。讨论了可卡因降低NA周转的可能机制。
