English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

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.

Neocortex- and hippocampus-specific deletion of Gabrg2 causes temperature-dependent seizures in mice