Glutamate receptor subunit GluA1 is necessary for long-term potentiation and synapse unsilencing, but not long-term depression in mouse hippocampus
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Xu_Glutamate receptor.pdf
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Author(s)
Selcher, Joel C.
Xu, Weifeng
Hanson, Jesse E.
Malenka, Robert C.
Madison, Daniel V.
Date Issued
November 2011
Journal
Brain Research
Publisher
Elsevier
Citation
Selcher, Joel C., Weifeng Xu, Jesse E. Hanson, Robert C. Malenka, and Daniel V. Madison. “Glutamate Receptor Subunit GluA1 Is Necessary for Long-Term Potentiation and Synapse Unsilencing, but Not Long-Term Depression in Mouse Hippocampus.” Brain Research 1435 (January 2012): 8–14.
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Author's final manuscript
Abstract
Receptor subunit composition is believed to play a major role in the synaptic trafficking of AMPA receptors (AMPARs), and thus in activity-dependent synaptic plasticity. To isolate a physiological role of GluA1-containing AMPARs in area CA3 of the hippocampus, pair recordings were performed in organotypic hippocampal slices taken from genetically modified mice lacking the GluA1 subunit. We report here that long-term potentiation (LTP) is impaired not only at active but also at silent synapses when the GluA1 subunit is absent. The GluA1 knockout mice also exhibited reduced AMPAR-mediated evoked currents between pairs of CA3 pyramidal neurons under baseline conditions suggesting a significant role for GluA1-containing AMPARs in regulating basal synaptic transmission. In two independent measures, however, long-term depression (LTD) was unaffected in tissue from these mice. These data provide a further demonstration of the fundamental role that GluA1-containing AMPARs play in activity-dependent increases in synaptic strength but do not support a GluA1-dependent mechanism for reductions in synaptic strength.
MIT Department
Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences
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DOI of Published Version
https://doi.org/10.1016/j.brainres.2011.11.029
