López-Colomé A M, Ortega A
Departamento de Neurociencias, Instituto de Fisiología Celular-UNAM.
Neurochem Res. 1997 Jun;22(6):679-85. doi: 10.1023/a:1027345808746.
The effect of L-glutamate (Glu) and its structural analogs N-methyl-D-aspartate (NMDA), kainate (KA) and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA), on the activation of p42 mitogen activated protein kinase (MAPK) was examined in cultured chick radial glia cells, namely retinal Muller cells and cerebellar Bergmann cells. Glu, NMDA, AMPA and KA evoked a dose and time dependent increase in MAPK activity. AMPA and KA responses were blocked by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) whereas NMDA responses were sensitive to 3-[(RS)-2-carboxypiperazin-4-yl)]-propyl-1-phosphonate (CPP) indicating that the increase in MAPK activity is mediated by AMPA/low affinity KA and NMDA subtypes of Glu receptors. The present findings open the possibility of a MAPK cascade involvement in the regulation of Glu-induced gene expression in radial glia.
在培养的鸡胚放射状胶质细胞,即视网膜穆勒细胞和小脑伯格曼细胞中,研究了L-谷氨酸(Glu)及其结构类似物N-甲基-D-天冬氨酸(NMDA)、海人藻酸(KA)和α-氨基-3-羟基-5-甲基-4-异恶唑丙酸(AMPA)对p42丝裂原活化蛋白激酶(MAPK)激活的影响。Glu、NMDA、AMPA和KA引起MAPK活性呈剂量和时间依赖性增加。AMPA和KA反应被6-氰基-7-硝基喹喔啉-2,3-二酮(CNQX)阻断,而NMDA反应对3-[(RS)-2-羧基哌嗪-4-基)]-丙基-1-膦酸(CPP)敏感,表明MAPK活性增加是由AMPA/低亲和力KA和NMDA亚型的Glu受体介导的。本研究结果揭示了MAPK级联参与调节放射状胶质细胞中Glu诱导的基因表达的可能性。