Fig. 5. Effects of propofol (Pro) and U0126 (U) on the  N -methyl-d-aspartate (NMDA)–stimulated phosphorylation of extracellular signal–regulated protein kinases 1 and 2 (ERK1/2;  A ), Elk-1 (  B ), and cyclic adenosine monophosphate response element–binding protein (CREB;  C ), and c-Fos expression (  D ) in cultured rat hippocampal neurons. Note that both propofol and U0126 blocked the NMDA-induced phosphorylation of ERK1/2, Elk-1, and CREB, without changing cellular levels of the three proteins. Propofol (10 μm) or U0126 (5 μm) was incubated 30 min before and during treatment with NMDA for 15 min (pERK1/2, pElk-1, and pCREB) or 30 min (c-Fos). Representative immunoblots are shown at left of the quantified data (mean ± SEM, n = 6). *  P < 0.05  versus basal levels. +  P < 0.05  versus NMDA alone. 

Fig. 5. Effects of propofol (Pro) and U0126 (U) on the  N -methyl-d-aspartate (NMDA)–stimulated phosphorylation of extracellular signal–regulated protein kinases 1 and 2 (ERK1/2;  A ), Elk-1 (  B ), and cyclic adenosine monophosphate response element–binding protein (CREB;  C ), and c-Fos expression (  D ) in cultured rat hippocampal neurons. Note that both propofol and U0126 blocked the NMDA-induced phosphorylation of ERK1/2, Elk-1, and CREB, without changing cellular levels of the three proteins. Propofol (10 μm) or U0126 (5 μm) was incubated 30 min before and during treatment with NMDA for 15 min (pERK1/2, pElk-1, and pCREB) or 30 min (c-Fos). Representative immunoblots are shown at left of the quantified data (mean ± SEM, n = 6). *  P < 0.05  versus basal levels. +  P < 0.05  versus NMDA alone. 

Close Modal

or Create an Account

Close Modal
Close Modal