Mori K, Suda N, Togashi H, Matsumoto M, Saito H, Yoshioka M
Department of Pharmacology, Hokkaido University School of Medicine, Sapporo, Japan.
Pharmacol Toxicol. 1999 Aug;85(2):98-102. doi: 10.1111/j.1600-0773.1999.tb00073.x.
In the present study, we investigated the effects of bifemelane on the reduction of hippocampal long-term potentiation after transient ischaemia. Bilateral common carotid arteries were clamped for 10 min. in halothane-anaesthetized rats. Thirty min. before occlusion, bifemelane (25 mg/kg, intraperitoneally) or saline was administered to the rats. Four days after occlusion, we measured long-term potentiation in Schaffer collateral-CA1 synapses and perforant path-dentate gyrus synapses in vivo. Long-term potentiation was significantly reduced in both the Schaffer collateral-CA1 and perforant path-dentate gyrus synapses in the saline-injected group. However bifemelane decreased the ischaemia-induced reduction of long-term potentiation in perforant path-dentate gyrus synapses, but not in Schaffer collateral-CA1 synapses. The findings suggest that bifemelane deserves further attention with regard to possible protective role in ischaemia.
在本研究中，我们调查了比芬美兰对短暂性缺血后海马长时程增强减弱的影响。在氟烷麻醉的大鼠中，双侧颈总动脉夹闭10分钟。在闭塞前30分钟，给大鼠腹腔注射比芬美兰（25毫克/千克）或生理盐水。闭塞后四天，我们在体测量了海马伞- CA1突触和穿通通路-齿状回突触的长时程增强。在注射生理盐水的组中，海马伞- CA1和穿通通路-齿状回突触的长时程增强均显著降低。然而，比芬美兰减少了穿通通路-齿状回突触中缺血诱导的长时程增强减弱，但在海马伞- CA1突触中没有。这些发现表明，比芬美兰在缺血方面可能的保护作用值得进一步关注。
