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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

Glutamatergic Plasticity by Synaptic Delivery of GluR-Blong-Containing AMPA Receptors

TL;DR: A study of GluR-B(long), a C-terminal splice variant of the Glu R-B subunit that mediates a GLUR-A-independent form of glutamatergic synaptic plasticity in the juvenile hippocampus is reported.
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Early remodeling of the neocortex upon episodic memory encoding

TL;DR: It is shown that episodic memory encoding elicits early remodeling of neocortical circuits in mouse brain and is identified as a critical regulator of encoding-induced hippocampal activation and long-term memory formation, which have important implications for understanding memory processing in healthy and diseased brain states.
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Loss of Hyperdirect Pathway Cortico-Subthalamic Inputs Following Degeneration of Midbrain Dopamine Neurons.

TL;DR: The data suggest that loss of dopamine triggers a maladaptive shift in the balance of synaptic excitation and inhibition in the STN, which contributes to parkinsonian activity and motor dysfunction.
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Caffeine-Mediated Presynaptic Long-Term Potentiation in Hippocampal CA1 Pyramidal Neurons

TL;DR: It is concluded that the CAFLTP requires the interaction of caffeine with presynaptic P1, P2 purinoreceptors, and ryanodine receptors and is caused by an increased probability of glutamate release at SC terminals.
Journal ArticleDOI

Cellular and System Biology of Memory: Timing, Molecules, and Beyond.

TL;DR: Cellular processes of synaptic plasticity, particularly functional and structural changes, and focus on timing events that are important for the initial memory acquisition are reviewed, as well as mechanisms of short- and long-term memory storage.
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.
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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