Dynamin-dependent NMDAR endocytosis during LTD and its dependence on synaptic state |
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| Authors: | Johanna?M?Montgomery Joel?C?Selcher Jesse?E?Hanson Email author" target="_blank">Daniel?V?MadisonEmail author |
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| Institution: | (1) Department of Molecular and Cellular Physiology, Beckman Center for Molecular and Genetic Medicine, Stanford University School of Medicine Stanford, 94305 CA, USA;(2) Department of Physiology, Faculty of Medical and Health Sciences, University of Auckland, New Zealand |
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| Abstract: | Background The N-methyl-D-aspartate (NMDA)-type glutamate receptor expressed at excitatory glutamatergic synapses is required for learning
and memory and is critical for normal brain function. At a cellular level, this receptor plays a pivotal role in triggering
and controlling synaptic plasticity. While it has been long recognized that this receptor plays a regulatory role, it was
considered by many to be itself immune to synaptic activity-induced plasticity. More recently, we and others have shown that
NMDA receptor-mediated synaptic responses can be subject to activity-dependent depression. |
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