Auxiliary subunits of the CKAMP family differentially modulate AMPA receptor properties
Paul Farrow,
Konstantin Khodosevich,
Yechiam Sapir,
Anton Schulmann,
Muhammad Aslam,
Yael Stern-Bach,
Hannah Monyer,
Jakob von Engelhardt
Affiliations
Paul Farrow
Synaptic Signalling and Neurodegeneration, German Cancer Research Center, Heidelberg, Germany; Synaptic Signalling and Neurodegeneration, German Center for Neurodegenerative Diseases, Bonn, Germany
Konstantin Khodosevich
Department of Clinical Neurobiology, Medical Faculty of Heidelberg University, Heidelberg, Germany; German Cancer Research Center, Heidelberg, Germany
Yechiam Sapir
Department of Biochemistry and Molecular Biology, Institute for Medical Research – Israel-Canada, The Hebrew University-Hadassah Medical School, Jerusalem, Israel
Anton Schulmann
Department of Clinical Neurobiology, Medical Faculty of Heidelberg University, Heidelberg, Germany; German Cancer Research Center, Heidelberg, Germany
Muhammad Aslam
Synaptic Signalling and Neurodegeneration, German Cancer Research Center, Heidelberg, Germany; Synaptic Signalling and Neurodegeneration, German Center for Neurodegenerative Diseases, Bonn, Germany
Yael Stern-Bach
Department of Biochemistry and Molecular Biology, Institute for Medical Research – Israel-Canada, The Hebrew University-Hadassah Medical School, Jerusalem, Israel
Hannah Monyer
Department of Clinical Neurobiology, Medical Faculty of Heidelberg University, Heidelberg, Germany
Synaptic Signalling and Neurodegeneration, German Cancer Research Center, Heidelberg, Germany; Synaptic Signalling and Neurodegeneration, German Center for Neurodegenerative Diseases, Bonn, Germany
AMPA receptor (AMPAR) function is modulated by auxiliary subunits. Here, we report on three AMPAR interacting proteins—namely CKAMP39, CKAMP52 and CKAMP59—that, together with the previously characterized CKAMP44, constitute a novel family of auxiliary subunits distinct from other families of AMPAR interacting proteins. The new members of the CKAMP family display distinct regional and developmental expression profiles in the mouse brain. Notably, despite their structural similarities they exert diverse modulation on AMPAR gating by influencing deactivation, desensitization and recovery from desensitization, as well as glutamate and cyclothiazide potency to AMPARs. This study indicates that AMPAR function is very precisely controlled by the cell-type specific expression of the CKAMP family members.
