ERK1/2-Dependent Phosphorylation of GABA$_{B1}$(S867/T872), Controlled by CaMKIIβ, Is Required for GABA$_{B}$ Receptor Degradation under Physiological and Pathological Conditions

Abstract

GABA$_{B}$ receptor-mediated inhibition is indispensable for maintaining a healthy neuronal excitation/inhibition balance. Many neurological diseases are associated with a disturbed excitation/inhibition balance and downregulation of GABA$_{B}$ receptors due to enhanced sorting of the receptors to lysosomal degradation. A key event triggering the downregulation of the receptors is the phosphorylation of S867 in the GABA$_{B1}$ subunit mediated by CaMKIIβ. Interestingly, close to S867 in GABA$_{B1}$ Show more