Grooms S Y, Jones L S
Department of Developmental Biology and Anatomy, University of South Carolina, School of Medicine, Columbia 29208.
Neuroreport. 1994 May 9;5(9):1102-4. doi: 10.1097/00001756-199405000-00020.
Effects of nitric oxide synthase (NOS) inhibitors on the induction of an in vitro model of kindling were investigated in the rat hippocampal slice. It has been reported that NMDA receptor activation stimulates NOS and guanosine 3',5'-cyclic monophosphate (cGMP) production and that the interruption of this pathway interferes with LTP in the CA1 hippocampal field. Because the induction of LTP and kindling both involve NMDA receptor activation, we tested the effects of NOS inhibitors on the genesis and initial rate of interictal-like spontaneous bursts in CA1 and CA3 of the rat hippocampal slice. Experimental groups were exposed to 100 microM methyl-L-arginine (active NOS inhibitor), nitro-L-arginine (active NOS inhibitor), or methyl-D-arginine (inactive isomer of the NOS inhibitor) for 1 h prior to in vitro kindling. These results indicate that rather than preventing the induction of kindling in this model of epileptogenesis, NOS inhibition may facilitate the initiation of interictal-like spontaneous bursts in the rat hippocampal slice.
在大鼠海马切片中研究了一氧化氮合酶（NOS）抑制剂对点燃体外模型诱导的影响。据报道，NMDA受体激活会刺激NOS和鸟苷3',5'-环磷酸（cGMP）的产生，并且该途径的中断会干扰海马CA1区的长时程增强（LTP）。由于LTP的诱导和点燃都涉及NMDA受体激活，我们测试了NOS抑制剂对大鼠海马切片CA1和CA3区发作间期样自发爆发的发生及初始速率的影响。在体外点燃前1小时，将实验组暴露于100微摩尔的甲基-L-精氨酸（活性NOS抑制剂）、硝基-L-精氨酸（活性NOS抑制剂）或甲基-D-精氨酸（NOS抑制剂的无活性异构体）中。这些结果表明，在这个癫痫发生模型中，NOS抑制可能不会阻止点燃的诱导，反而可能促进大鼠海马切片中发作间期样自发爆发的起始。
