Freedman L S, Judge M E, Quartermain D
Pharmacol Biochem Behav. 1982 Aug;17(2):187-91. doi: 10.1016/0091-3057(82)90068-5.
Cycloheximide (CXM), a protein synthesis inhibitor, has been shown to result in a marked inhibition of central catecholamine (CA) synthetic mechanisms at doses that cause amnesia in animals. Unlike other inhibitors of CA synthesis no significant depletion of whole brain NE or DA concentrations was observed 0.75, 1, 2, 3, 4, 6, 17, or 24 hours after administration of CXM (120 mg/kg) to C57BL/6J mice. In order to investigate the underlying basis of maintenance of CA levels in face of CA synthesis inhibition, the effects of CXM on in vitro release of 3H-NE was studied in mouse hypothalamic slices. CXM, in a dose related manner, significantly inhibited the potassium stimulated release of NE from hypothalamic slices. Anisomycin, another protein synthesis inhibitor, similarly inhibited NE release. These studies further document the effects of protein synthesis inhibitors on CA mechanisms and suggest that disruption of CA biochemistry may play a role in the amnesia observed after administration of protein synthesis inhibitors.
放线菌酮（CXM）是一种蛋白质合成抑制剂，已表明在导致动物失忆的剂量下，它会显著抑制中枢儿茶酚胺（CA）的合成机制。与其他CA合成抑制剂不同，给C57BL/6J小鼠注射CXM（120mg/kg）后0.75、1、2、3、4、6、17或24小时，未观察到全脑NE或DA浓度有明显降低。为了研究在CA合成受抑制情况下CA水平维持的潜在基础，在小鼠下丘脑切片中研究了CXM对3H-NE体外释放的影响。CXM以剂量相关的方式显著抑制了下丘脑切片中钾刺激的NE释放。另一种蛋白质合成抑制剂茴香霉素同样抑制NE释放。这些研究进一步证明了蛋白质合成抑制剂对CA机制的影响，并表明CA生物化学的破坏可能在蛋白质合成抑制剂给药后观察到的失忆中起作用。
