Postsynaptic Signaling and Plasticity Mechanisms

By M. Sheng, M. J. Kim. Science, 2002

749 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/e07b8f4d7c337d8ed0558c86c9ef4050bac3c38c

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

1. R. Malenka
2. A. Citri
3. M. Sheng
4. Joseph E LeDoux
5. Michael D. Ehlers
6. T. Tada
7. B. Philpot
8. C. Zuccato

In Molecular Biology

1. R. Malenka
2. M. Sheng
3. A. Citri
4. Joseph E LeDoux
5. Michael D. Ehlers
6. B. Philpot
7. T. Tada
8. H. Lipp

Citations in the corpus

• Arc/Arg3.1 is essential for the consolidation of synaptic plasticity and memories. (2006, positive): “Enduring forms of LTP and memory are dependent on mRNA and protein synthesis and rely on rearrangements in the structure and molecular composition of protein networks at synapses (Goelet et al., 1986; Sheng and Kim, 2002; Pocklington et al., 2006).”
• Synaptic Plasticity: Multiple Forms, Functions, and Mechanisms (2008, background): “…expanded to include synapses that already contained AMPARs and has led to a large investigative effort into the molecular mechanisms regulating the trafficking of AMPARs (Bredt and Nicoll, 2003; Collingridge et al, 2004; Malinow and Malenka, 2002; Sheng and Kim, 2002; Song and Huganir, 2002).”
• Normal huntingtin function: an alternative approach to Huntington's disease (2005, background): “One key molecule in synaptic transmission is PSD-95 (postsynaptic density protein 95), a member of the membrane-associated guanylate kinase (MAGUK) family of proteins that binds the NMDA ( N -methyl- D -aspartate) and kainate receptors at the postsynaptic densit”
• The Role of Palmitoylation in Functional Expression of Nicotinic α7 Receptors (2004, background): “With the recent evidence that LGIC assembly and trafficking are key processes underlying long-lasting changes in synaptic strength (Barry and Ziff, 2002; Malinow and Malenka, 2002; Sheng and Kim, 2002), the palmitoylation of LGIC subunits may have a role in regulating these processes.”
• Molecular mechanisms of dendritic spine morphogenesis. (2006, background): “Although small in size (up to a few microns in length), spines appear to contain all the essential molecules and organelles involved in postsynaptic signaling and plasticity [1,2].”
• Conditional Knock-Out of Kir4.1 Leads to Glial Membrane Depolarization, Inhibition of Potassium and Glutamate Uptake, and Enhanced Short-Term Synaptic Potentiation (2007, background): “…function, such as alterations in the probability of transmitter release, whereas changes in EPSC amplitude appear to involve modification of the postsynaptic terminal responsiveness (Sheng and Kim, 2002; Stevens, 2004), both of which can be modulated by extracellular ion and transmitter levels.”
• The Role of N-Methyl-d-Aspartate (NMDA) Receptors in Pain: A Review (2003, background): “These proteins, such as neuronal NO synthase, SynGAP, and SPAR, may participate in downstream signaling by NMDARs (47).”
• Structural plasticity and memory (2004, background): “The PSD includes receptors, channels and signalling molecules that couple synaptic activity with postsynaptic biochemistr”
• Activity level controls postsynaptic composition and signaling via the ubiquitin-proteasome system (2003, background): “Much of this remodeling occurs at the postsynaptic density (PSD), a specialized biochemical apparatus containing glutamate receptors and associated scaffolding proteins that organize signal transduction pathways at the postsynaptic membran”