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. Author manuscript; available in PMC: 2010 Apr 7.
Published in final edited form as: J Neurosci. 2009 Oct 7;29(40):12702–12710. doi: 10.1523/JNEUROSCI.1166-09.2009

Fig. 3.

Fig. 3

Stimulation of CREB-dependent gene transcription requires activation of NR2B-containing NMDARs and L-type Cavs. Induction of 4xCRE transcription by 10 μM forskolin (a) or 3 mM 8-Br-cAMP (b) was blocked by the NMDAR antagonists AP5 (100 μM) or ifenprodil (10 μM) and by the L-type Cav antagonists verapamil (100 μM) or nifedipine (100 μM). (c) Activation of NMDARs with NMDA (30 μM + 10 μM glycine) induced 4xCRE transcription that was sensitive to AP5 (100 μM) or ifenprodil (10 μM), but not to Cav antagonists. Similarly, NMDA-stimulated 4xCRE expression was blocked by Bapta-free acid (Bapta-FA; 3 mM) or by pre-treating neurons with 10 μM Bapta-AM. The L-type Cav antagonist, nifedipine (100 μM), did not reduce NMDA-stimulated 4xCRE transcription. ***, p< 0.001 from agonist-induced response; ns = not significantly different from NMDA alone.