Work

CaMKII modulates sodium current in neurons from epileptic Scn2a mutant mice

Year: 2017

Type: article

Abstract: Significance Epilepsy is a neurological disorder affecting approximately 1% of the world population. Mutations within genes encoding voltage-gated channels are the most frequently identified cause of monogenic epilepsies. Variable expressivity is a common feature of many epilepsies, suggesting that modifier genes make significant contributions to clinical phenotype. Here, we report an investigation of the molecular basis for strain-dependent seizure severity in the Scn2a Q54 epileptic mice. We show strain-dependent differences in pyramidal cell excitability correlate with divergent properties of voltage-gated sodium channels that could be explained by differences in calcium/calmodulin protein kinase II (CaMKII)-dependent modulation of neuronal sodium channels. These findings suggest that strain-dependent sodium channel modulation by CaMKII in Scn2a Q54 mice influences excitatory neuronal networks.

Source: Proceedings of the National Academy of Sciences

DOI: 10.1073/pnas.1615774114

Authors: Christopher H. Thompson, Nicole A. Hawkins, Jennifer A. Kearney, Alfred L. George

Institution: Northwestern University

Language: English

Topic: Ion channel regulation and function

Subfield: Molecular Biology

Field: Biochemistry, Genetics and Molecular Biology

Domain: Life Sciences

SDG: Good health and well-being

Open Access status: green

Funders: Epilepsy Foundation, National Institutes of Health, National Institute of Neurological Disorders and Stroke