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Journal ArticleDOI

Long-Term Potentiation--A Decade of Progress?

Robert C. Malenka, +1 more
- 17 Sep 1999 - 
- Vol. 285, Iss: 5435, pp 1870-1874
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TLDR
A simple model is described that unifies much of the data that previously were viewed as contradictory about the molecular mechanisms of this long-lasting increase in synaptic strength in the hippocampus.
Abstract
Long-term potentiation of synaptic transmission in the hippocampus is the leading experimental model for the synaptic changes that may underlie learning and memory. This review presents a current understanding of the molecular mechanisms of this long-lasting increase in synaptic strength and describes a simple model that unifies much of the data that previously were viewed as contradictory.

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Citations
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Journal ArticleDOI

Long-term potentiation of intrinsic excitability in LV visual cortical neurons.

TL;DR: Activity-dependent plasticity in intrinsic excitability could greatly expand the computational power of individual neurons as well as serve as an important information storage mechanism.
Journal ArticleDOI

Activity-driven postsynaptic translocation of CaMKII.

TL;DR: An overview of recent progress in postsynaptic CaMKII anchoring is provided and its implication in synaptic plasticity and the etiology and potential treatments of neurological diseases is discussed.
Journal ArticleDOI

Effects of dendritic morphology on CA3 pyramidal cell electrophysiology: a simulation study

TL;DR: It is reported for the first time that differences in dendritic structure within the same morphological class can have a dramatic influence on the firing rate and firing mode (spiking versus bursting and type of bursting).
Journal ArticleDOI

Decreased NR1, NR2A, and SAP102 transcript expression in the hippocampus in bipolar disorder

TL;DR: It is proposed that the NMDA receptor signaling complex, including the intracellular machinery that is coupled to theNMDA receptor subunits, is abnormal in the hippocampus in bipolar disorder.
Journal ArticleDOI

Hebbian and neuromodulatory mechanisms interact to trigger associative memory formation

TL;DR: Direct in vivo evidence is provided supporting the idea that a parallel mechanism involving neuromodulation and Hebbian processes is both necessary and sufficient to trigger synaptic strengthening and behavioral associative memory formation and suggesting that combined HeBBian and neurmodulatory processes interact to engage associative aversive learning.
References
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Journal ArticleDOI

A synaptic model of memory: long-term potentiation in the hippocampus

TL;DR: The best understood form of long-term potentiation is induced by the activation of the N-methyl-d-aspartate receptor complex, which allows electrical events at the postsynaptic membrane to be transduced into chemical signals which, in turn, are thought to activate both pre- and post Synaptic mechanisms to generate a persistent increase in synaptic strength.
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Long-lasting potentiation of synaptic transmission in the dentate area of the anaesthetized rabbit following stimulation of the perforant path.

TL;DR: The after‐effects of repetitive stimulation of the perforant path fibres to the dentate area of the hippocampal formation have been examined with extracellular micro‐electrodes in rabbits anaesthetized with urethane.
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Synaptic Activity and the Construction of Cortical Circuits

TL;DR: The sequential combination of spontaneously generated and experience-dependent neural activity endows the brain with an ongoing ability to accommodate to dynamically changing inputs during development and throughout life.
Journal ArticleDOI

Dendritic spine changes associated with hippocampal long-term synaptic plasticity

TL;DR: After induction of long-lasting (but not short-lasting) functional enhancement of synapses in area CA1, new spines appear on the postsynaptic dendrite, whereas in control regions on the same dendrites or in slices where long-term potentiation was blocked, no significant spine growth occurred.
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Deficient Hippocampal Long-Term Potentiation in α-Calcium-Calmodulin Kinase II Mutant Mice

TL;DR: W Whole cell recordings reveal that postsynaptic mechanisms, including N-methyl-D-aspartate (NMDA) receptor function, are intact and are therefore a suitable model for studying the relation between LTP and learning processes.
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