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. Author manuscript; available in PMC: 2010 Apr 21.
Published in final edited form as: J Neurosci Res. 2009 Sep;87(12):2632–2644. doi: 10.1002/jnr.22103

Fig. 1.

Fig. 1

The activation of ERK1/2 and CREB declines following in vitro maturation. Cortical neurons were stimulated by 50 mM KCl (a, b, and c) or 50 uM NMDA2 uM glycine (b and c) at DIV3 and 14. (a). KCl stimulated ERK1/2 phosphorylation at both DIV 3 and 14. For (b) and (c), neurons were pretreated with CNQX and nifedipine, or CNQX and APV, as indicated, for 30min before the stimulation by KCl (along with APV and CNQX) and NMDA/glycine (along with nifedipine and CNQX). Samples were collected 15 min after stimulation. The signal of p-ERK1/2 was normalized with total ERK1/2 or beta-actin. The signal of p-CREB was normalized with beta-actin. Data are average +/− SD (n=5 for each group).