Neocortical LTD via coincident activation of presynaptic NMDA and cannabinoid receptors.
By Per Jesper Sjöström, Gina G. Turrigiano, Sacha B. Nelson. Neuron, 2003
641 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Cognitive Neuroscience
View Paper: https://www.semanticscholar.org/paper/445a91725b80f2a4742564d4a89ee59b36666169
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
- Wulfram Gerstner
- D. Feldman
- Pierre Yger
- Niraj S. Desai
- Matthieu Gilson
- A. Watt
- Kenneth D. Harris
- Friedemann Zenke
In Cognitive Neuroscience
- Wulfram Gerstner
- Pierre Yger
- D. Feldman
- Matthieu Gilson
- Friedemann Zenke
- Niraj S. Desai
- Kenneth D. Harris
- A. Watt
Citations in the corpus
- Spike timing-dependent plasticity: from synapse to perception. (2006, background): “aptic NMDARs to induce LTD (96), as blocking the degradation of endocannabinoids was found to widen the LTD window.”
- Models of Metaplasticity: A Review of Concepts (2015, background): “…experimental results, it is commonly assumed that synaptic changes triggered by Hebbian plasticity protocols are rather fast (Bliss and Lomo, 1973; Sjöström et al., 2001, 2003; Wang et al., 2005), occurring in the timescale of minutes or faster, while metaplasticity or homeostatic changes are…”
- Synaptic Mechanisms for Plasticity in Neocortex (2009, background): “STDP mechanisms are surprisingly diverse, involving NMDA-LTP and NMDA-LTD at some synapses (Froemke et al. 2005), NMDA-LTP and CB1-LTD at others (Sjostrom et al. 2003, Bender et al. 2006b, Nevian & Sakmann 2006) and mGluR-LTD at others (Egger et al. 1999).”
- Distinct coincidence detectors govern the corticostriatal spike timing‐dependent plasticity (2010, background): “A growing body of evidence indicates that a single coincidence detector model cannot explain STDP at different synapses (Karmarkar & Buonomano, 2002; Sjöström et al. 2003; Bender et al. 2006; Nevian & Sakmann, 2006; Tzounopoulos et al. 2007).”
- Distribution of cannabinoid receptors in the central and peripheral nervous system. (2005, neutral): “actions on glutamatergic transmission in cortex (Sjostrom et al. 2003).”
- Calcium-based plasticity model explains sensitivity of synaptic changes to spike pattern, rate, and dendritic location (2012, background): “Another G protein-coupled LTD induction pathway involves retrograde signaling by endocannabinoids (15, 24), whose efficiency is greatly modulated by postsynaptic calcium (15, 25, 26).”
- Gain in sensitivity and loss in temporal contrast of STDP by dopaminergic modulation at hippocampal synapses (2009, background): “For example, visual cortical synapses exhibit postsynaptic t-LTP and presynaptic t-LTD, probably through the interaction between presynaptic NMDA receptor signaling and retrograde endocannabinoid signaling (50, 51).”
- Differential Roles of NR2A and NR2B-Containing NMDA Receptors in Cortical Long-Term Potentiation and Long-Term Depression (2004, background): “LTD requires the activation of postsynaptic NMDARs It has been reported that NR2B-containing NMDARs are located presynaptically (Woodhall et al., 2001) and that presynaptic NMDARs may be important in the induction of LTD in cerebellum (Casado et al., 2002) and neocortex (Sjostrom et al., 2003).”
- Synaptic Plasticity: Multiple Forms, Functions, and Mechanisms (2008, background): “…Neuropsychopharmacology REVIEWS REVIEW by a spike-timing-dependent protocol (Sjostrom et al, 2003) but does not depend on postsynaptic activation of mGluRs and surprisingly, requires coincident activation of presynaptic NMDARs.”
- Spike-timing dependent plasticity (2010, background): “Consistent with this finding, the induction of timing-dependent depression at layer-5 synapses in visual cortex results in a long-term down regulation of short-term depression through an apparent decrease of the probability of release (Sjöström et al., 2003), which is in effect anti-RSE.”
- Reinforcement learning with modulated spike timing dependent synaptic plasticity. (2007, background): “…release and presynaptic NMDARs), possibly using different calcium sources for induction (internal stores instead of extracellular calcium admitted through postsynaptic NMDARs), and perhaps with a different site of expression (Bender et al. 2006; Nevian and Sakmann 2006; Sjöström et al. 2003, 2004).”
- A History of Spike-Timing-Dependent Plasticity (2011, background): “Furthermore, the temporal asymmetry as well as the mechanistic underpinnings of spike-timingdependent LTD (Sjöström et al., 2003) are indistinguishable from LTD triggered by pairing presynaptic input with subthreshold depolarization (Sjöström et al., 2004).”
- Pyramidal Neuron Conductance State Gates Spike-Timing-Dependent Plasticity (2010, result): “…is consistent with recent experiments that indicate that t-LTP and t-LTD involve separate calcium sources and coincidence detection mechanisms (Sjöström et al., 2003, 2004; Bender et al., 2006; Chevaleyre et al., 2006; Duguid and Sjöström, 2006; Nevian and Sakmann, 2006; Rodríguez-Moreno…”
- Frontiers in Synaptic Neuroscience Synaptic Neuroscience (positive): “How general a means of stabilization is this “redistribution of synaptic efficacy” phenomenon? The complementary effect (reduced short-term depression) has been observed after timingdependent LTD in layer 5 neocortex (Sjostrom et al., 2003), and both effects have been observed at hippocampal CA1 syn”
- Connectivity reflects coding: a model of voltage-based STDP with homeostasis (2010, background): “In light of the results on LTD in layer V neocortical neuron”