Activity level controls postsynaptic composition and signaling via the ubiquitin-proteasome system

By Michael D. Ehlers. Nature Neuroscience, 2003

772 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/c6ecd6051dbfe0bc4b7ad8fed2a2a6e487cd0cb3

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In Cellular and Molecular Neuroscience

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Citations in the corpus

Rapid Redistribution of Synaptic PSD-95 in the Neocortex In Vivo (2006, background): “However, this explanation is likely not sufficient because PSD-95 binding partners are also unstable [23,59], with half-lives at synapses on the order of minutes to hours [60,61].”
Homeostatic plasticity in the developing nervous system (2004, background): “The changes in receptor accumulation produced by synaptic scaling are accompanied by changes in the turnover and synaptic localization of many postsynaptic proteins that are involved in clustering receptors at synapses, indicating that altered activity produces a coordinated set of changes in recept”
NMDA receptor trafficking in synaptic plasticity and neuropsychiatric disorders (2007, background): “The number and subunit composition of synaptic NMDARs are regulated not only by stimulus-dependent gene expression and protein synthesis, but also by activity-dependent protein degradation by the ubiquitin–proteasome syste”
Effects of secreted oligomers of amyloid β‐protein on hippocampal synaptic plasticity: a potent role for trimers (2006, methodology): “Because postnatal day (P)8–9 mice have immature synapses that are not capable of following HFS, we modified our LTP protocol to induce a chemical LTP by using picrotoxin, glycine and low Mg2+ to elevate spontaneous synaptic activity in brain slices (Neuhoff et al. 1999; Lu et al. 2001; Ehlers, 2003)”
The cell biology of synaptic plasticity: AMPA receptor trafficking. (2007, background): “However, PSD-95 ubiquitination is not detectable in all conditions (Bingol & Schuman 2004, Ehlers 2003), possibly owing to subtle differences in experimental conditions.”
Regulation of NMDA Receptor Subunit Expression and Its Implications for LTD, LTP, and Metaplasticity (2008, background): “activity-dependent regulation can be prevented by proteasome inhibitors (Ehlers, 2003).”
Regulation of NMDA receptor trafficking by amyloid-β (2005, result): “Although we did not observe an increase in extrasynaptic staining for NMDA receptors, these observations are consistent with other published accounts of NMDA receptor redistributio”
Neuroligins determine synapse maturation and function. (2006, methodology): “Second, dramatic homeostatic compensatory changes in postsynaptic protein expression are also known to occur in cultured cells in vitro (Ehlers, 2003).”
Sensitive Periods in the Development of the Brain and Behavior (2004, background): “If the fundamental changes require synapse formation or elimination, then the loss of key mechanisms that support these processes would end the sensitive period (Huberman & McAllister, 2002; Katz & Shatz, 1996; Fox & Zahs, 1994), and if the fundamental changes rely on structural stabilization of sel”
Miniature neurotransmission stabilizes synaptic function via tonic suppression of local dendritic protein synthesis. (2006, neutral): “Moreover, other studies have suggested that synaptic modifications underlying scaling induced by AP blockade might arise by mechanisms targeting the preexisting complement of synaptic proteins rather than the regulated synthesis of new components (O’Brien et al., 1998; Ehlers, 2003 ).”
Ubiquitination regulates PSD-95 degradation and AMPA receptor surface expression. (2003, background): “…al., 2001; Moss et al., 2002), future studsynaptic activity can alter the levels of a variety of PSD ies should focus on a role for ubiquitination and degraproteins in cultured rat neurons through the ubiquitin- dation of PSD-95 in memory formation and stability. proteasome system (Ehlers, 2003).”
The Self-Tuning Neuron: Synaptic Scaling of Excitatory Synapses (2008, background): “Chronic changes in activity regulate the synaptic content of a large array of synaptic proteins in addition to glutamate receptors, suggesting that the overall protein composition of the postsynaptic density is adjusted by ongoing activity (Ehlers, 2003).”