GIRK Channel Loss of Function Increases Dendritic Excitability in a Mouse Model of GNB1 Encephalopathy
This study demonstrates that the GNB1 p.I80T mutation in mice causes GNB1 encephalopathy-like symptoms by impairing GIRK channel function, which reduces synaptic inhibition and increases dendritic excitability, a mechanism that can be therapeutically targeted by GIRK activators to alleviate seizures and learning deficits.