Epileptogenic mechanisms in focal cortical dysplasia (FCD) remain elusive as no animal models faithfully recapitulate FCD seizures that have distinct electrographic features and a wide range of semiologies. Given that DEPDC5 plays significant roles in focal epilepsies with FCD, we used in utero electroporation (IUE) with clustered regularly interspaced short palindromic repeats (CRISPR) gene deletion to create focal somatic Depdc5 deletion in the rat embryonic brain. Animals developed spontaneous seizures with focal pathological and electroclinical features highly clinically relevant to FCD IIA, paving the way to understand its pathogenesis and develop mechanistic-based therapies.
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