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. Author manuscript; available in PMC: 2012 Jul 1.
Published in final edited form as: Glia. 2011 May 4;59(7):1084–1093. doi: 10.1002/glia.21181

Figure 4. Adenosine A1 receptor activation enhances NMDAR current via tyrosine phosphorylation of Src Kinase in dnSNARE mice.

Figure 4

(A–C), Slices from dnSNARE mice were incubated in CCPA (100nM) for 1hour or pre-incubated with Src kinase inhibitor PP2 (10 µM) 30 min. (A) Representative western blots using anti-Src, anti-p-Src, anti-p-NR2B antibodies. The levels of tyrosine phosphorylation of Src kinase and NR2B were significantly increased by incubation with CCPA. PP2 prevented these CCPA induced increases in phosphorylation. (n=3, *p<0.05 control compared with CCPA; #p<0.05 CCPA compared with CCPA/PP2). (B) Representative western blots using anti-NR2B antibody to detect the total and surface expression of NR2B. CCPA significantly increased surface expression of NR2B and the increase was inhibited by preincubation of PP2 (n=4, *p<0.05). (C) In the presence of TTX, CCPA significantly increased tyrosine phosphorylation of Src and NR2B, as well as the surface expression of NR2B (n=3, *p<0.05). (D) In slices from dnSNARE, NMDA components of mixed mEPSC significantly increased after CCPA incubation and the increase was blocked by PP2 (control: 13 cells from 7 mice, CCPA: 11 cells from 7 mice, CCPA/PP2: 11 cells from 6 mice).