Matthew S. Scarnati

GIRK Channel Loss of Function Increases Dendritic Excitability in a Mouse Model of GNB1 Encephalopathy

It is shown that a pathogenic variant of the G protein subunit Gβ1 impairs activation of neuronal G-protein-coupled inwardly rectifying potassium (GIRK) channels by inhibitory synaptic GABAB receptors, which leads to increased dendritic excitability and longer duration dendritic calcium spikes in mouse hippocampal neurons in response to stimulation of synaptic inputs.