In a mouse model of focal cortical dysplasia (FCD) type II, we found that mTOR-dependent excessive growth of excitatory synapses strongly drives the mutated neurons with ultralow intrinsic excitability to be hyperexcitable in the network. Moreover, the excitability of mutated neurons could be reduced by the activation of GABAb receptors via a presynaptic mechanism. Wang et al., 2025.
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