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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

Molecular Mechanisms of Early and Late LTP

TL;DR: Current knowledge about early and late phases of LTP will be reviewed, and current knowledge about constitutively active PKMζ is reviewed.
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Prominence of Direct Entorhinal–CA1 Pathway Activation in Sensorimotor and Cognitive Tasks Revealed by 2-DG Functional Mapping in Nonhuman Primate

TL;DR: Findings indicate a remarkable invariance in hippocampal activation under conditions of varied content, varied process, and varied mode of response and an heretofore-unappreciated preferential engagement of the direct rather than the trisynaptic pathway during performance of a wide range of behavioral tasks.
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A CalDAG-GEFI/Rap1/B-Raf Cassette Couples M1Muscarinic Acetylcholine Receptors to the Activation of ERK1/2

TL;DR: A novel signaling pathway for M1 mAChR is defined, where increases in Ca2+ and diacylglycerol stimulate the sequential activation of CalDAG-GEFI, Rap1, and B-Raf, resulting in the activation of MEK and ERK1/2.
Journal ArticleDOI

Neural plasticity: consequences of stress and actions of antidepressant treatment

TL;DR: The literature is presented demonstrating altered plasticity in response to stress, and evidence that chronic antidepressant treatment can reverse or block the effects, and even induce neural piasiicity-iike responses.
Journal ArticleDOI

Molecular and cellular mechanisms underlying the cognitive deficits associated with neurofibromatosis 1.

TL;DR: It is suggested that the learning disabilities associated with neurofibromatosis 1 are caused by excessive Ras activity that leads to increased γ-aminobutyric acid (GABAA) inhibition and to decreased long-term potentiation.
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.
Journal ArticleDOI

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.
Journal ArticleDOI

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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