Activation of epidermal growth factor receptor inhibits KCNQ2/3 current through two distinct pathways: membrane PtdIns(4,5)P2 hydrolysis and channel phosphorylation.

ABSTRACT: KCNQ2/3 currents are the molecular basis of the neuronal M currents that play a critical role in neuron excitability. Many neurotransmitters modulate M/KCNQ currents through their G-protein-coupled receptors. Membrane PtdIns(4,5)P2 hydrolysis and channel phosphorylation are two mechanisms that have been proposed for modulation of KCNQ2/3 currents. In this study, we studied regulation of KCNQ2/3 currents by the epidermal growth factor (EGF) receptor, a member of another family of membrane receptors, receptor tyrosine kinases. We demonstrate here that EGF induces biphasic inhibition of KCNQ2/3 currents in human embryonic kidney 293 cells and in rat superior cervical ganglia neurons, an initial fast inhibition and a later slow inhibition. Additional studies indicate that the early and late in

SUBMITTER: Jia Q 

PROVIDER: S-EPMC6672518 | biostudies-literature | 2007 Mar

REPOSITORIES: biostudies-literature