کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4325457 | 1614004 | 2012 | 7 صفحه PDF | دانلود رایگان |

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.
► AMPA receptor subunit composition plays a major role in trafficking of those receptors in and out of the synaptic membrane and as a result, synaptic plasticity.
► We confirm that active excitatory synapses from hippocampus of a GluA1 AMPA receptor subunit null mouse, cannot undergo long-term potentiation, and show for the first time that silent synapses cannot be activated in this tissue as well.
► The amplitude of quantal excitatory postsynaptic currents is decreased in this knockout tissue.
► We also show for the first time that long-term depression is induced normally in this knockout tissue.
Journal: Brain Research - Volume 1435, 30 January 2012, Pages 8–14