A mechanism for the Hebb and the anti-Hebb processes underlying learning and memory.

By John E. Lisman. 1989

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Citations in the corpus

Born to Learn: the Inspiration, Progress, and Future of Evolved Plastic Artificial Neural Networks (2017, background): “Those advances in the 1970s and 1980s lead to the mathematical formulation of synaptic learning dynamics (Lisman, 1989; Brown et al., 1990), e.g. the BCM rule, inspired by the cat’s visual cortex (Bienenstock et al., 1982), and the Oja’s rule (Oja, 1982).”
Tag-Trigger-Consolidation: A Model of Early and Late Long-Term-Potentiation and Depression (2008, neutral): “. Detailed biophysical models of LTP and LTD describe calcium dynamics and Calcium/Calmodulin-Dependent Protein Kinase II (CaMKII) phosphorylation during the induction and early phase of LTP”
The spike timing dependence of plasticity (2012, background): “These are as follows: (1) NMDA receptor (NMDAR)-dependent LTP and (2) NMDARdependent LTD, in which correlated presynaptic release and postsynaptic depolarization trigger calcium influx through postsynaptic NMDARs (and voltage-sensitive calcium channels, VSCCs).”
Biologically Plausible Error-Driven Learning Using Local Activation Differences: The Generalized Recirculation Algorithm (1996, background): “On the other hand, a proposed mechanism that depends only on the level of postsynaptic [Ca”], (Lisman 1989), has received some recent empirical support (reviewed in Lisman 1994; Bear and Malenka 1994).”
Regulation of AMPA receptor endocytosis by a signaling mechanism shared with LTD (2000, background): “Thus a critical question is whether, like NMDAR-dependent LTD in the hippocampus, NMDAR activation can lead to the triggering of AMPAR endocytosis, and if so, what signal transduction pathway mediates this effect? The most prominent hypothesis for the triggering of NMDAR-dependent LTD proposes that ”
The tempotron: a neuron that learns spike timing–based decisions (2006, result): “Recent reports provide support for the long-standing hypothesi”
Spike-Timing Dependence of Structural Plasticity Explains Cooperative Synapse Formation in the Neocortex (2012, background): “A biochemical mechanism underlying this assumption could be the activation of a signaling pathway when a specific number of activated CaMKII molecules is reached [39].”
Spike Timing Dependent Plasticity: A Consequence of More Fundamental Learning Rules (2010, unknown): “The calcium assumption is based on experimental evidence (Cummings et al., 1996; Yang et al., 1999) and has been previously suggested in models of calcium-dependent kinase-phosphatase systems in postsynaptic spines (Lisman, 1989).”
Eligibility Traces and Plasticity on Behavioral Time Scales: Experimental Support of NeoHebbian Three-Factor Learning Rules (2018, background): “On the molecular level, the striatal three-factor plasticity depended on NMDA, CaMKII, protein synthesis, and dopamine D1 receptors (Yagishita et al., 2014; Shindou et al., 2018).”