BARP regulates the dynamics of voltage-dependent Ca2+ channel complexes at dendritic spine

The dynamics of voltage-dependent Ca2+ channel (VDCC) complexes are crucial for neuronal excitability, neurotransmitter release, and neuronal morphology. Recently, VDCC beta-anchoring and -regulatory protein (BARP) was identified as a novel regulator of VDCC activity via the interaction with VDCC β subunits. However, its physiological significance has been largely unknown. In this study, we reveal that BARP regulates the dynamics of VDCC complexes at dendritic spine. Fluorescence recovery after photobleaching assay revealed that BARP accelerates the fluorescence recovery of both VDCC α1 and β subunits at dendritic spine. BARP forms VDCC α1/β/BARP complex via BARP Region II and this ternary complex is important for accelerating the dynamics of VDCC complex. Cell surface labeling assay showed that BARP reduces the expression level of VDCC α1 subunit at the plasma membrane. Pharmacological studies suggest that BARP decreases the insertion of VDCC complex into the plasma membrane. These results suggest that BARP regulates the Ca2+ signaling at dendritic spine by altering the dynamics of VDCC complexes.