Agonist-dependent endocytosis of γ-aminobutyric acid type A (GABAA) receptors revealed by a γ2(R43Q) epilepsy mutation

Abstract

Background: Modulation of GABAA receptors trafficking is critical for controlling inhibitory neurotransmission. Results: A point mutation or agonist application, both affecting the GABAA receptor extracellular domain, has an effect on receptor endocytosis. Conclusion: Endocytosis of GABA A receptors is linked to agonist-induced conformational changes. Significance: This represents one of the few reports demonstrating an influence of extracellular effectors on GABAA receptor trafficking. © 2013 by The American Society for Biochemistry and Molecular Biology, Inc.