Dysmorphic neurons with ultralow intrinsic excitability are paradoxically hyperexcitable in neural network in a mouse model of focal cortical dysplasia type II

Together, these findings indicate that excessive excitatory synaptic inputs prevail over reduced intrinsic excitability in dysmorphic neurons, leading to hyperexcitability in FCDII. Furthermore, they strongly suggest GABA_B receptors as a potential therapeutic target for FCDII.