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. Author manuscript; available in PMC: 2016 Mar 1.
Published in final edited form as: J Neurochem. 2014 Nov 10;132(6):742–755. doi: 10.1111/jnc.12956

Figure 3. Production of LMW-E2F1 is mediated by NR2A/2B-containing NMDAR stimulation.

Figure 3

a. Immunoblot of subcellular fractions from rat cortical cultures (DIV21) treated for 20 hours with HIVMDM or mock supernatants. For indicated samples, NMDAR antagonist MK801 (10μM) was added to cultures 30 minutes prior to supernatant treatment. Coomassie-stained gel serves as a loading control. b,c. Rat cortical cultures at DIV21 were pre-treated for 1 hour with different NMDAR subunit inhibitors (Table, c) followed by HIVMDM treatment. Conantokin G (CoG, 10μM), which blocks NR2A/2B-containing NMDARs prevented the production of LMW-E2F1, while Ifenprodil (Ifn, 10μM), which blocks NR2B/2B-containing NMDARs, and Zinc (Zn, 500nM) which blocks NR2A-containing NMDARs, had no effect on HIVMDM-induced formation of LMW-E2F1. Coomassie-stained gel serves as a loading control.