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Updated: Apr 26, 2026
Preparation and Implantation of Electrodes for Electrically Kindling VGAT-Cre Mice to Generate a Model for Temporal Lobe Epilepsy
Published on: August 17, 2021
Selective suppression of excessive GluN2C expression rescues early epilepsy in a tuberous sclerosis murine model
N Lozovaya1, S Gataullina1, T Tsintsadze2
11] INSERM U901, INMED, Parc Scientifique et Technologique de Luminy 163, route de Luminy-BP 13, 13273 Marseille Cedex 09, France [2] UMR901, Aix-Marseille University, 58 Boulevard Charles Livon, 13284 Marseille, France [3] INSERM U1129; University Paris Descartes, CEA, Gif sur Yvette, 149 Rue de Sèvres, 75015 Paris, France [4].
Abstract:
Tuberous sclerosis complex (TSC), caused by dominant mutations in either TSC1 or TSC2 tumour suppressor genes is characterized by the presence of brain malformations, the cortical tubers that are thought to contribute to the generation of pharmacoresistant epilepsy. Here we report that tuberless heterozygote Tsc1(+/-) mice show functional upregulation of cortical GluN2C-containing N-methyl-D-aspartate receptors (NMDARs) in an mTOR-dependent manner and exhibit recurrent, unprovoked seizures during early postnatal life (
