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. 2006 Aug 9;26(32):8339–8351. doi: 10.1523/JNEUROSCI.0472-06.2006

Figure 5.

Figure 5.

NMDAR activation regulates total GluR2 mRNA abundance but does alter mRNA stability. a, Representative Northern blot analysis of mRNA samples from control (cntrl) and NMDA-treated cortical neurons (see Materials and Methods). b, Quantitation of data. Brief stimulation with NMDA (50 μm, 60 s) in the presence of CNQX reduced cellular GluR1 and GluR2, but not NR1 or GAPDH, mRNA content in neurons, assessed at 30 min after initiation of drug application. c–e, Representative Northern blots and decay rates of GluR2 (c), NR1 (d), and GAPDH (e) mRNAs in the presence of the transcriptional inhibitor actinomycin D or after NMDA treatment in the presence of actinomycin D. c, In the presence of actinomycin D, GluR2 mRNA exhibited a relatively rapid rate of constitutive decay relative to that of NR1 (d) or GAPDH (e) mRNA. NMDA did not significantly alter the constitutive decay of GluR2, NR1, or GAPDH mRNA observed in the presence of actinomycin D, indicating no detectable effect on mRNA stability. Error bars represent SEMs for four independent experiments (**p ≤ 0.01).