Author
Listed:
- Xinglong Gu
(Synapse and Neural Circuit Research Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 35 Convent Drive, 3C1000, Bethesda, Maryland 20892, USA)
- Xia Mao
(Synapse and Neural Circuit Research Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 35 Convent Drive, 3C1000, Bethesda, Maryland 20892, USA)
- Marc P. Lussier
(Receptor Biology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 35 Convent Drive, 2C903, Bethesda, Maryland 20892, USA
Present address: Département de Chimie, Université du Québec à Montréal, Montréal, Québec, Canada H3C 3P8)
- Mary Anne Hutchison
(Synapse and Neural Circuit Research Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 35 Convent Drive, 3C1000, Bethesda, Maryland 20892, USA)
- Liang Zhou
(Synapse and Neural Circuit Research Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 35 Convent Drive, 3C1000, Bethesda, Maryland 20892, USA)
- F. Kent Hamra
(Cecil H. & Ida Green Center for Reproductive Biology Sciences, University of Texas Southwestern Medical Center in Dallas)
- Katherine W. Roche
(Receptor Biology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 35 Convent Drive, 2C903, Bethesda, Maryland 20892, USA)
- Wei Lu
(Synapse and Neural Circuit Research Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 35 Convent Drive, 3C1000, Bethesda, Maryland 20892, USA)
Abstract
Regulation of AMPA receptor (AMPAR)-mediated synaptic transmission is a key mechanism for synaptic plasticity. In the brain, AMPARs assemble with a number of auxiliary subunits, including TARPs, CNIHs and CKAMP44, which are important for AMPAR forward trafficking to synapses. Here we report that the membrane protein GSG1L negatively regulates AMPAR-mediated synaptic transmission. Overexpression of GSG1L strongly suppresses, and GSG1L knockout (KO) enhances, AMPAR-mediated synaptic transmission. GSG1L-dependent regulation of AMPAR synaptic transmission relies on the first extracellular loop domain and its carboxyl-terminus. GSG1L also speeds up AMPAR deactivation and desensitization in hippocampal CA1 neurons, in contrast to the effects of TARPs and CNIHs. Furthermore, GSG1L association with AMPARs inhibits CNIH2-induced slowing of the receptors in heterologous cells. Finally, GSG1L KO rats have deficits in LTP and show behavioural abnormalities in object recognition tests. These data demonstrate that GSG1L represents a new class of auxiliary subunit with distinct functional properties for AMPARs.
Suggested Citation
Xinglong Gu & Xia Mao & Marc P. Lussier & Mary Anne Hutchison & Liang Zhou & F. Kent Hamra & Katherine W. Roche & Wei Lu, 2016.
"GSG1L suppresses AMPA receptor-mediated synaptic transmission and uniquely modulates AMPA receptor kinetics in hippocampal neurons,"
Nature Communications, Nature, vol. 7(1), pages 1-18, April.
Handle:
RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms10873
DOI: 10.1038/ncomms10873
Download full text from publisher
Citations
Citations are extracted by the
CitEc Project, subscribe to its
RSS feed for this item.
Cited by:
- Caleigh M Azumaya & Emily L Days & Paige N Vinson & Shaun Stauffer & Gary Sulikowski & C David Weaver & Terunaga Nakagawa, 2017.
"Screening for AMPA receptor auxiliary subunit specific modulators,"
PLOS ONE, Public Library of Science, vol. 12(3), pages 1-23, March.
- Amanda M. Perozzo & Jochen Schwenk & Aichurok Kamalova & Terunaga Nakagawa & Bernd Fakler & Derek Bowie, 2023.
"GSG1L-containing AMPA receptor complexes are defined by their spatiotemporal expression, native interactome and allosteric sites,"
Nature Communications, Nature, vol. 14(1), pages 1-15, December.
Corrections
All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms10873. See general information about how to correct material in RePEc.
If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.
We have no bibliographic references for this item. You can help adding them by using this form .
If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.
For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .
Please note that corrections may take a couple of weeks to filter through
the various RePEc services.