Erratum: NF-κB functions in synaptic signaling and behavior

Nat. Neurosci. 6, 1072–1078 (2003)

Due to a typesetting error in the Fig. 3 legend, the symbol μ was mistakenly printed as the letter 'm'. This led to erroneous concentration descriptions for reagents in panels c and d. The corrected legend appears below.

Figure 3 Ca²⁺-dependent pathway of NF-κB activation. (c,d) Cultures were unstimulated or stimulated with bicuculline (50 μM, + 4-aminopyridine 5 μM), in the presence or absence of intracellular Ca²⁺ chelators (EGTA, BAPTA or Br₂-BAPTA), and subjected to EMSA or reporter assay. All cultures were preincubated in activity-inhibitors, which were washed out before loading with intracellular Ca²⁺ buffers and stimulation. (c) Averaged data from five separate EMSA experiments; error bars represent one s.e.m. Br₂-BAPTA (50 μM) did not significantly attenuate NF-κB activation compared to bicuculline alone; EGTA (50 μM or 100 μM (2× EGTA)) modestly decreased NF-κB activation (t-test, P ≤ 0.10) and BAPTA effectively eliminated NF-κB activation (P ≤ 0.001). (d) Cultures were co-infected with an NF-κB-reporter gene (κB-luc) or an NFAT-reporter gene (NFAT-luc) and, to permit normalization, a constitutively expressed β-galactosidase. Data shown are averaged replicates from four separate assays. Br₂-BAPTA (50 μM) did not significantly attenuate NF-κB activation compared to bicuculline alone. EGTA (50 μM or 100 μM (2× EGTA)) marginally, but not significantly (P = 0.3327), decreased κB-luciferase activity, and BAPTA effectively eliminated NF-κB transcriptional activation (P ≤ 0.001). Transcriptional activation from the NFAT-responsive element was significantly inhibited by either BAPTA or EGTA (P ≤ 0.005 for both).