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Ion channel gating and kinase regulation of N-methyl-D-aspartate receptor 1 activity are fundamental mechanisms that govern synaptic plasticity. In this study, we showed that two mutant models (16p11.2del and Δdisc1) that recapitulate aspects of human cognitive disorders shared a similar defect in N-methyl-D-aspartate receptor 1-dependent synaptic function. Our results demonstrate that the expression of small-conductance potassium channels (SK2 or KCa2.2) was significantly upregulated in the hippocampus and prefrontal cortex of 16p11.2del and 129S:Δdisc1 mutant mice. Likewise, both mutant strains exhibited an impairment of T286 phosphorylation of calcium-calmodulin-dependent kinase II (CaMKII) in the hippocampus and prefrontal cortex. In vivo neural recordings revealed that increased SK2 expression and impaired T286 phosphorylation of CaMKII coincide with a prolonged interspike interval in the hippocampal cornu ammonis-1 (CA1) field for both 16p11.2del and 129S:Δdisc1 mutant mice. These findings suggest that alteration of small conductance channels and T286 phosphorylation of CaMKII are likely shared factors underlying behavioral changes in these two genetic mouse models.

Upregulated SK2 Expression and Impaired CaMKII Phosphorylation Are Shared Synaptic Defects Between 16p11.2del and 129S:Δdisc1 Mutant Mice