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. 2011 May 4;31(18):6627–6638. doi: 10.1523/JNEUROSCI.0203-11.2011

Figure 8.

Figure 8.

Involvement of NR2B-containing NMDA receptors in TBOA-induced phosphorylation of p38 MAPK and dephosphorylation of ERK1/2 and CREB. A, p38 MAPK inhibitor, SB 203580 (SB) (5 μm), significantly decreased LTP inhibition by the glutamate reuptake inhibitor TBOA (15 μm). B, Calpeptin (Cal) (100 μm), significantly decreased LTP inhibition by TBOA (15 μm). C, D, Western blots of the indicated phosphoproteins (p- prefix) in cultured hippocampal neurons. E, F, Summary histograms quantifying relative immunoreactivity. C, E, Neurons were untreated or treated with TBOA (20 μm) for 1, 3, 6 or 16 h or without TBOA for 16 h. D, F, Hippocampal neurons were exposed as indicated to TBOA without or with the NR2B-selective NMDAR inhibitors ifenprodil (Ifen) and Ro-6981 (Ro) (0.5 μm) or calpain inhibitor calpeptin (100 μm) for 6 h and then analyzed with the indicated antibodies. Data (means ± SEM) are from at least four independent batches of cultured neurons.