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. Author manuscript; available in PMC: 2012 Jan 7.
Published in final edited form as: Nature. 2011 Jun 15;475(7354):91–95. doi: 10.1038/nature10130

Figure 3. Ketamine blocks NMDAR spontaneous activity, reduces the level of eEF2 phosphorylation, and strengthens synaptic responses.

Figure 3

a, Representative western blots from hippocampal primary cultures. b, (left) Densitometric analysis of peEF2 (normalized-total eEF2). Data expressed as mean percentage±SEM. TTX alone does not alter peEF2 while AP5 or ketamine, with or without TTX, significantly decreases peEF2 as assessed by t-test analysis (*P<0.05). (right) Application of 1, 5 and 50 μM of ketamine produces dose-dependent decreases in peEF2 assessed by t-test analysis (*P<0.05). c, Representative traces of NMDAR spontaneous activity after application of 1, 5 and 50 μM. d, Quantification of charge transfer (10 sec) reveals significant effects (*P<0.05) for all ketamine concentrations compared to control (n=6-16) assessed by t-test analysis (*P<0.05). e, Field potential slopes are plotted as a function of time. Representative field potential traces, (average 2-min) are shown during baseline (1) and at 45-min (2). The asterisk refers to significantly different field potentials values (*P<0.05). For statistical analysis we used two-way repeated ANOVA with Bonferroni post-hoc analysis. The drug-time interaction was significant (F143,1430=6.723 P<0.001).