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. 2015 Apr 23;10(4):e0123718. doi: 10.1371/journal.pone.0123718

Fig 2. Effect of transfection with ATP binding-impaired αCaMKII K42M mutant under different conditions.

Fig 2

(A) Example pairs of AMPAR EPSC traces at –65 mV from nontransfected cells and cells transfected with wild type or mGFP-αCaMKII K42M variants in control ACSF or in the presence of 100 μM DL-APV or 1 μM TTX. (B) Each dot compares the EPSC in untransfected and transfected cells. Overexpression of wild-type mGFP-αCaMKII has no effect on AMPAR EPSCs in normal media (top right). Overexpression of kinetically dead mGFP-αCaMKII K42M mutant leads to suppression of AMPAR EPSCs in normal media (top left), but effect is blocked by APV or TTX (bottom panels). Thick solid lines correspond to linear fits having the stated slope.