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Neocortex- and hippocampus-specific deletion of Gabrg2 causes temperature-dependent seizures in mice
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Neocortex- and hippocampus-specific deletion of Gabrg2 causes temperature-dependent seizures in mice
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Journal Article
Neocortex- and hippocampus-specific deletion of Gabrg2 causes temperature-dependent seizures in mice
2021
Overview
Mutations in the
GABRG2
gene encoding the γ-aminobutyric acid (GABA) A receptor gamma 2 subunit are associated with genetic epilepsy with febrile seizures plus, febrile seizures plus, febrile seizures, and other symptoms of epilepsy. However, the mechanisms underlying
Gabrg2
-mediated febrile seizures are poorly understood. Here, we used the Cre/loxP system to generate conditional knockout (CKO) mice with deficient
Gabrg2
in the hippocampus and neocortex. Heterozygous CKO mice (
Gabrg2
fl/wt
Cre
+
) exhibited temperature-dependent myoclonic jerks, generalised tonic-clonic seizures, increased anxiety-like symptoms, and a predisposition to induce seizures. Cortical electroencephalography showed the hyperexcitability in response to temperature elevation in
Gabrg2
fl/wt
Cre
+
mice, but not in wild-type mice.
Gabrg2
fl/wt
Cre
+
mice exhibited spontaneous seizures and susceptibility to temperature-induced seizures. Loss of neurons were observed in cortical layers V–VI and hippocampus of
Gabrg2
fl/wt
Cre
+
mice. Furthermore, the latency of temperature- or pentylenetetrazol-induced seizures were significantly decreased in
Gabrg2
fl/wt
Cre
+
mice compared with wild-type mice. In summary,
Gabrg2
fl/wt
Cre
+
mice with
Gabrg2
deletion in the neocortex and hippocampus reproduce many features of febrile seizures and therefore provide a novel model to further understand this syndrome at the cellular and molecular level.
Publisher
Nature Publishing Group UK,Springer Nature B.V,Nature Publishing Group
Subject
