Wallin Camilla, Abbas Abdul-Karim, Tranberg Mattias, Weber Stephen G, Wigström Holger, Sandberg Mats
Department of Medical Biophysics, University of Göteborg, Medicinaregatan 11, S-405 30 Göteborg, Sweden.
Neurochem Res. 2003 Feb;28(2):281-91. doi: 10.1023/a:1022381318126.
N-Methyl-D-aspartate (NMDA)-receptor stimulation evoked a selective and partly delayed elevated efflux of glutathione, phosphoethanolamine, and taurine from organotypic rat hippocampus slice cultures. The protein kinase inhibitors H9 and staurosporine had no effect on the efflux. The phospholipase A2 inhibitors quinacrine and 4-bromophenacyl bromide, as well as arachidonic acid, a product of phospholipase A2 activity, did not affect the stimulated efflux. Polymyxin B, an antimicrobal agent that inhibits protein kinase C, and quinacrine in high concentration (500 microM), blocked efflux completely. The stimulated efflux after but not during NMDA incubation was attenuated by a calmodulin antagonist (W7) and an anion transport inhibitor (DNDS). Omission of calcium increased the spontaneous efflux with no or small additional effects by NMDA. In conclusion, NMDA receptor stimulation cause an increased selective efflux of glutathione, phosphoethanolamine and taurine in organotypic cultures of rat hippocampus. The efflux may partly be regulated by calmodulin and DNDS sensitive channels.
N-甲基-D-天冬氨酸（NMDA）受体刺激可诱发大鼠海马脑片培养物中谷胱甘肽、磷酸乙醇胺和牛磺酸的选择性且部分延迟的外流增加。蛋白激酶抑制剂H9和星形孢菌素对外流无影响。磷脂酶A2抑制剂奎纳克林和4-溴苯甲酰溴，以及磷脂酶A2活性产物花生四烯酸，均不影响刺激引起的外流。多粘菌素B（一种抑制蛋白激酶C的抗菌剂）和高浓度（500微摩尔）的奎纳克林可完全阻断外流。NMDA孵育后而非孵育期间的刺激外流，被钙调蛋白拮抗剂（W7）和阴离子转运抑制剂（DNDS）减弱。去除钙会增加自发外流，NMDA对此无额外影响或仅有微小影响。总之，NMDA受体刺激导致大鼠海马脑片培养物中谷胱甘肽、磷酸乙醇胺和牛磺酸的选择性外流增加。外流可能部分受钙调蛋白和DNDS敏感通道调节。
