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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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Excitability changes induced in the human motor cortex by weak transcranial direct current stimulation.

TL;DR: Transcranial electrical stimulation using weak current may be a promising tool to modulate cerebral excitability in a non‐invasive, painless, reversible, selective and focal way.
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Neurotrophins: roles in neuronal development and function.

TL;DR: Neurotrophins regulate development, maintenance, and function of vertebrate nervous systems, and control synaptic function and synaptic plasticity, while continuing to modulate neuronal survival.
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Memory--a century of consolidation.

TL;DR: This review examines the progress made over the century in understanding the time-dependent processes that create the authors' lasting memories.
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LTP and LTD: an embarrassment of riches.

TL;DR: This work reviews those forms of LTP and LTD for which mechanisms have been most firmly established and examples are provided that show how these mechanisms can contribute to experience-dependent modifications of brain function.
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Neuronal plasticity: increasing the gain in pain.

TL;DR: Here, a conceptual framework for the contribution of plasticity in primary sensory and dorsal horn neurons to the pathogenesis of pain is developed, identifying distinct forms of Plasticity, which are term activation, modulation, and modification, that by increasing gain, elicit pain hypersensitivity.
References
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Journal ArticleDOI

Postsynaptic NMDA receptor-mediated calcium accumulation in hippocampal CA1 pyramidal cell dendrites.

TL;DR: It is reported that brief high frequency stimulus trains produce a transient component spatially localized to dendritic areas near activated afférents, which directly confirm the calcium rise predicted by NMDA receptor models of LTP induction.
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Bidirectional Control of Quantal Size by Synaptic Activity in the Hippocampus

TL;DR: Analysis of strontium-induced asynchronous release of quanta from stimulated synapses revealed that long-term potentiation and long- term depression in the CA1 region of the mammalian hippocampus are associated with an increase and a decrease, respectively, in quantal size.
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Presynaptic component of long-term potentiation visualized at individual hippocampal synapses

TL;DR: Monitoring at synapses between cultured rat hippocampal neurons by measuring the differential uptake of antibodies that recognize the intraluminal domain of the synaptic vesicle protein synaptotagmin shows Vesicular cycling increased markedly during glutamate-induced long-term potentiation.
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Synaptic plasticity: hippocampal LTP

TL;DR: The past year has seen further evidence advanced on both sides of the presynaptic/postsynaptic locus of expression debate, without an obvious path to reconcile the two views.
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