Article
CaMKII modulates sodium current in neurons from epileptic Scn2a mutant mice.
Proceedings of the National Academy of Sciences of the United States of America - 14 Feb 2017
Thompson Christopher H, Hawkins Nicole A, Kearney Jennifer A, George Alfred L
Abstract excerpt
Monogenic epilepsies with wide-ranging clinical severity have been associated with mutations in voltage-gated sodium channel genes. In the Scn2aQ54 mouse model of epilepsy, a focal epilepsy phenotype is caused by transgenic expression of an engineered NaV1.2 mutation displaying enhanced persistent sodium current. Seizure frequency and other phenotypic features in Scn2aQ54 mice depend on genetic background. We...
Topics
- Animals
- Calcium-Calmodulin-Dependent Protein Kinase Type 2
- Epilepsy
- HEK293 Cells
- Hippocampus
- Humans
- Membrane Potentials
- Mice, Inbred C57BL
- Mice, Inbred Strains
- Mice, Transgenic
- Mutation
- NAV1.2 Voltage-Gated Sodium Channel
- Neurons
- Patch-Clamp Techniques