Investigating Sodium Channels in Infantile Epilepsy
Faculty Mentor Information
Dr. James Groome, Idaho State University; and Dr. Lizbeth de la Cruz, Idaho State University
Presentation Date
7-16-2026
Abstract
Developmental epilepsy syndromes are severe neurological disorders that remain difficult to investigate. Many are caused by mutations in voltage-gated sodium channels, which alter channel function, disrupt neuronal excitability, and lead to abnormal electrical activity. Our research aims to develop a computational model that quantitatively predicts how sodium channel dysfunction contributes to epileptic activity in a noninvasive manner. To achieve this, we combine electrophysiological measurements of wild-type and mutant voltage-gated sodium channels obtained using the cut-open voltage-clamp technique in Xenopus oocytes expressing the corresponding channel mRNAs with immunohistochemistry and confocal microscopy to optimize a primary-secondary antibody binding system and generate spatial maps of sodium channel distribution along cortical axons in the mouse cortex. These complementary electrophysiological and imaging datasets are integrated into NEURON, a computational modeling platform that simulates neuronal behavior based on experimentally determined channel properties. By incorporating both functional and spatial information, our model will provide a more biologically realistic representation of neuronal excitability and improve our understanding of how sodium channel dysfunction contributes to developmental epilepsy. This work was done as part of our VIP course "Neurobiology across the Lifespan" and supported by ISU SPARC grant award " Modeling neuronal excitability in developmental epilepsy syndrome".
Investigating Sodium Channels in Infantile Epilepsy
Developmental epilepsy syndromes are severe neurological disorders that remain difficult to investigate. Many are caused by mutations in voltage-gated sodium channels, which alter channel function, disrupt neuronal excitability, and lead to abnormal electrical activity. Our research aims to develop a computational model that quantitatively predicts how sodium channel dysfunction contributes to epileptic activity in a noninvasive manner. To achieve this, we combine electrophysiological measurements of wild-type and mutant voltage-gated sodium channels obtained using the cut-open voltage-clamp technique in Xenopus oocytes expressing the corresponding channel mRNAs with immunohistochemistry and confocal microscopy to optimize a primary-secondary antibody binding system and generate spatial maps of sodium channel distribution along cortical axons in the mouse cortex. These complementary electrophysiological and imaging datasets are integrated into NEURON, a computational modeling platform that simulates neuronal behavior based on experimentally determined channel properties. By incorporating both functional and spatial information, our model will provide a more biologically realistic representation of neuronal excitability and improve our understanding of how sodium channel dysfunction contributes to developmental epilepsy. This work was done as part of our VIP course "Neurobiology across the Lifespan" and supported by ISU SPARC grant award " Modeling neuronal excitability in developmental epilepsy syndrome".