Increased seizure susceptibility and cortical malformation in β-catenin mutant mice

VE Campos, M Du, Y Li - Biochemical and biophysical research …, 2004 - Elsevier
VE Campos, M Du, Y Li
Biochemical and biophysical research communications, 2004Elsevier
β-Catenin has been implicated in epilepsy because of its altered post seizure expression
and the role of Wnt2 signaling in autism. To determine β-catenin's role in seizure
susceptibility, we injected penetylenetetrazol intraperitoneally in β-catenin cerebral cortex-
and hippocampus-specific knockout mice. We then analyzed the latency, number, and
duration of four phases of seizure behaviors:(I) non-seizure activity,(II) myoclonic jerks,(III)
generalized clonic seizures, and (IV) tonic seizures. The latencies to both death and Phase …
β-Catenin has been implicated in epilepsy because of its altered post seizure expression and the role of Wnt2 signaling in autism. To determine β-catenin’s role in seizure susceptibility, we injected penetylenetetrazol intraperitoneally in β-catenin cerebral cortex- and hippocampus-specific knockout mice. We then analyzed the latency, number, and duration of four phases of seizure behaviors: (I) non-seizure activity, (II) myoclonic jerks, (III) generalized clonic seizures, and (IV) tonic seizures. The latencies to both death and Phase IV were significantly reduced in mutant mice. Mutant mice also spent significantly more time in Phases III and IV and showed significantly less time in the non-convulsive state (Phase I). Nissl and gold chloride staining indicated that the knockout mice had underdeveloped cortices, lacked a corpus callosum, and were missing hippocampal structures. This suggests that dysfunction of β-catenin-mediated signaling pathways in mice leads to cortical malformation and increased seizure susceptibility.
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