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. 2012 Jan 17;287(11):8495–8506. doi: 10.1074/jbc.M111.323915

FIGURE 9.

FIGURE 9.

Pharmacological antagonism of the NMDA receptor prevents acute and prolonged effects of CaMKII inhibition. A, average integral of fluorescent intensity from 0 to 1200 s (mean ± S.E., n = 3–6) reflecting calcium influx in control neurons, or neurons subjected to treatment with tat-CN21 alone or in combination with 20 μm MK-801 or in combination with a prior synaptic NMDA-R blockade. To block synaptic NMDA-Rs before tat-CN21 treatment, 10 μm bicuculline was applied to allow synaptic activity, followed by the addition of 20 μm MK-801 to inhibit the synaptic NMDA-Rs opened as a result of this synaptic activity. *, p < 0.05 compared with control; #, p < 0.05 compared with tat-CN21 (one-way ANOVA, post hoc Dunnett's test). B, neuronal death (mean ± S.E., n = 4–24) after 24 h of treatment with 10 μm tat-CN21 alone or in the presence of 20 μm MK-801, 10 μm ifenprodil, 1 μm memantine, or 200 nm tetrodotoxin (TTX). *, p < 0.05 compared with control; #, p < 0.05 compared with tat-CN21 (one-way ANOVA, post hoc Dunnett's test).