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. Author manuscript; available in PMC: 2012 Aug 25.
Published in final edited form as: Neuroscience. 2011 May 19;189:305–315. doi: 10.1016/j.neuroscience.2011.05.027

Figure 3. Both endogenous and exogenous ADAR2 cleavage occurs through the activation of NMDA receptors.

Figure 3

A. Cortical neurons expressing Flag-ADAR2 were either untreated (lane 1) or treated with glutamate (lane 2), and the glutamate and APV (lane 3) glutamate and CNQX (lane 4) glutamate with APV and CNQX (lane 5), glutamate and nifedipine (lane 6), glutamate with APV and nifedipine (lane 7) and glutamate with CNQX and nifedipine (lane8).

B. Cortical neurons expressing Flag-ADAR2 were either not treated or treated with AMPA, NMDA or glutamate. Nuclear extracts were analyzed using western blotting using anti-Flag antibody. Lane 1 untreated, lane 2 AMPA 20)µM, lane 3 NMDA 20µM and lane 4 glutamate 20µM for 1 hr.

C. Cortical neurons were either not stimulated or stimulated with NMDA or glutamate. Nuclear extracts were prepared and analyzed using SDS-PAGE followed by western blotting. Endogenous ADAR2 was detected using anti-ADAR2 antibody. Untreated (lane), NMDA (lane 2), glutamate (lane 3).

D. Cortical neurons expressing Flag-ADAR2 were either not treated or treated with 100µM AMPA for I hr. Nuclear extracts were prepared and analyzed using SDS-PAGE followed by western blotting using anti-Flag antibody. Untreated (lane1), 100µM AMPA (lane 2).