Absence of bidirectional plasticity at PF-PC synapses when the CaMKII concentration is equal in wild-type and knockout mice: kinase and phosphatase activities at different calcium concentrations. The figure shows simulation results which indicate that the suggested explanation of the experimental observations by33 (Fig. 1) does not occur for higher calcium concentrations if the CaMKII concentration at knockout mice is not reduced due to a compensatory upregulation of α CaMKII. Low calcium concentrations that induce LTP in wild-type mice (solid) lead to LTD in Camk2b knockout mice (dashed), and vice versa. However, we observe that we do not see the inversion of plasticity for higher calcium concentrations if we do not reduce the CaMKII concentration for the knockout mice. Thus, we would not get the same results as in Fig. 4. The only modification was keeping the CaMKII concentration equal for both types of mice, and not reducing it for knockout mice. (A) Average concentrations of CaMKIIac (blue) and PP2Bac (red) as a function of average concentrations of pulsed calcium at 1 Hz for 300 s. (B) Average concentrations of unphosphorylated and phosphorylated AMPA receptors (red and blue, respectively) in response to the same stimulation protocols. The figures show average concentrations of CaMKIIac, PP2Bac and AMPA receptors in the presence of calcium signals applied at 1 Hz for 300 s. The panels show the average concentrations of these compounds during simulations that last 6000 s, that is, continue for 5700 s after the offset of the 300 s stimulation.