NMDA receptor trafficking in synaptic plasticity and neuropsychiatric disorders

By D. Purpura, C. G. Lau, R. Zukin. Nature Reviews Neuroscience, 2007

1,198 citations recorded by the source corpus.

Subfields: Cell Biology, Cellular and Molecular Neuroscience, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/0504eeb9bf8454ba842100e1c61d9defb05aea16

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Citations in the corpus

Synaptic plasticity and addiction (2007, background): “A subunit switch between particular NMDAR subunits can also up- or downregulate NMDAR-mediated synaptic currents so that more or less Ca 2+ will enter the postsynaptic neuron during receptor activation, thereby altering the induction of synaptic plasticity”
Epigenomic profiling reveals DNA-methylation changes associated with major psychosis. (2008, background): “and proteins associated with mitochondrial function and oxidative stress responses were the most altered group.(25) Traditional etiological studies of complex disease, both genetic and epigenetic, have tended to investigate discrete regions of DNA in isolation.”
Cellular and synaptic mechanisms of anti-NMDA receptor encephalitis (2010, background): “Central to these neurological functions is the proper synaptic localization and trafficking of the excitatory glutamate NMDA and AMPA receptors (Lau and Zukin, 2007; Shepherd and Huganir, 2007).”
TrkB signalling pathways in LTP and learning (2009, background): “This provides another dynamic and potentially powerful mechanism for regulating synaptic efficacy and remodellin”
Circuit-based framework for understanding neurotransmitter and risk gene interactions in schizophrenia. (2008, background): “The possibilities include reduction in the concentrations of the co-agonists, glycine [38,39] and D-serine levels [40], elevated levels of endogenous antagonists (NAAG/kynurenic acid) [41,42], alterations in the redox state of the NMDA channel [43] or reduced channel expression or trafficking [13,44”
Dysconnection in Schizophrenia: From Abnormal Synaptic Plasticity to Failures of Self-monitoring (2009, background): “cell membrane as well as their endocytosis, and these mechanisms are known to be highly relevant for pathophysiological processes in several brain diseases.(30) Furthermore, the conductance properties of NMDARs depend on their phos-”
Metaplasticity: tuning synapses and networks for plasticity (2008, background): “It has been suggested that NMDAR activation results in LTD of NMDAR currents (LTD NMDAR ), which are crucial for the induction of conventional LTD and LTP and are known to be highly plastic in their function and localization (for reviews, see Ref”
NMDA receptor subunit diversity: impact on receptor properties, synaptic plasticity and disease (2013, background): “Lateral diffusion (1), exocytosis and endocytosis (2) and”
Regulation of NMDA Receptor Subunit Expression and Its Implications for LTD, LTP, and Metaplasticity (2008, background): “Readers are directed to other recent reviews for a more in-depth perspective on the functions and regulation of NMDARs (CullCandy and Leszkiewicz, 2004; Kopp et al., 2007; Lau and Zukin, 2007) and for additional hypotheses regarding the induction of metaplasticity (Abraham, 2008).”