Brain natriuretic peptide constitutively downregulates P2X3 receptors by controlling their phosphorylation state and membrane localization
Conclusions:
We demonstrated that in mouse trigeminal neurons endogenous BNP acts on NPR-A receptors to determine constitutive depression of P2X3 receptor function. Tonic inhibition of P2X3 receptor activity by BNP/NPR-A/PKG pathways occurs via two distinct mechanisms: P2X3 serine phosphorylation and receptor redistribution to non-raft membrane compartments. This novel mechanism of receptor control might be a target for future studies aiming at decreasing dysregulated P2X3 receptor activity in chronic pain.
Source: Molecular Pain - Category: Molecular Biology Authors: Anna MarchenkovaSandra VilottiElsa FabbrettiAndrea Nistri Source Type: research
More News: Brain | Chronic Pain | Depression | Ganglions | Molecular Biology | Neurology | Pain | Study