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Numerous genetic variants associated with MEF2C are linked to autism, intellectual disability (ID) and schizophrenia (SCZ) - a heterogeneous collection of neurodevelopmental disorders with unclear pathophysiology. MEF2C is highly expressed in developing cortical excitatory neurons, but its role in their development remains unclear. We show here that conditional embryonic deletion of Mef2c in cortical and hippocampal excitatory neurons (Emx1-lineage) produces a dramatic reduction in cortical network activity in vivo, due in part to a dramatic increase in inhibitory and a decrease in excitatory synaptic transmission. In addition, we find that MEF2C regulates E/I synapse density predominantly as a cell-autonomous, transcriptional repressor. Analysis of differential gene expression in Mef2c mutant cortex identified a significant overlap with numerous synapse- and autism-linked genes, and the Mef2c mutant mice displayed numerous behaviors reminiscent of autism, ID and SCZ, suggesting that perturbing MEF2C function in neocortex can produce autistic- and ID-like behaviors in mice.
Dendritic spine dynamics are thought to be substrates for motor learning and memory, and altered spine dynamics often lead to impaired performance. Here, we describe an exception to this rule by studying mice lacking paired immunoglobulin receptor B (PirB-/-). Pyramidal neuron dendrites in PirB-/- mice have increased spine formation rates and density. Surprisingly, PirB-/- mice learn a skilled reaching task faster than wild-type (WT) littermates. Furthermore, stabilization of learning-induced spines is elevated in PirB-/- mice. Mechanistically, single-spine uncaging experiments suggest that PirB is required for NMDA receptor (NMDAR)-dependent spine shrinkage. The degree of survival of newly formed spines correlates with performance, suggesting that increased spine stability is advantageous for learning. Acute inhibition of PirB function in M1 of adult WT mice increases the survival of learning-induced spines and enhances motor learning. These results demonstrate that there are limits on motor learning that can be lifted by manipulating PirB, even in adulthood.
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