Journal ArticleDOI
Locally distributed synaptic potentiation in the hippocampus
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TLDR
The data presented here indicate that long-term potentiation can be communicated between synapses on neighboring neurons by means of a diffusible messenger, which provides a mechanism for the cooperative strengthening of proximal synapses and may underlie a variety of plastic processes in the nervous system.Abstract:
The long-lasting increase in synaptic strength known as long-term potentiation has been advanced as a potential physiological mechanism for many forms of both developmental and adult neuronal plasticity. In many models of plasticity, intercellular communication has been proposed to account for observations in which simultaneously active neurons are strengthened together. The data presented here indicate that long-term potentiation can be communicated between synapses on neighboring neurons by means of a diffusible messenger. This distributed potentiation provides a mechanism for the cooperative strengthening of proximal synapses and may underlie a variety of plastic processes in the nervous system.read more
Citations
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Journal ArticleDOI
Long-Term Potentiation--A Decade of Progress?
TL;DR: 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.
Journal ArticleDOI
Neurotrophins and neuronal plasticity.
TL;DR: A role for NTs as selective retrograde messengers that regulate synaptic efficacy is suggested, based on evidence that NT synthesis is rapidly regulated by neuronal activity and that NTs are released in an activity-dependent manner from neuronal dendrites.
Journal ArticleDOI
Synaptic Modification by Correlated Activity: Hebb's Postulate Revisited
Guo-Qiang Bi,Mu-ming Poo +1 more
TL;DR: Spike timing-dependent modifications, together with selective spread of synaptic changes, provide a set of cellular mechanisms that are likely to be important for the development and functioning of neural networks.
Journal ArticleDOI
Induction of plasticity in the human motor cortex by paired associative stimulation.
TL;DR: It is proposed that the induced plasticity may represent a signature of associative long-term potentiation of cortical synapses or closely related neuronal mechanisms in the human cortex.
Journal ArticleDOI
Synaptic plasticity: LTP and LTD
Mark F. Bear,Robert C. Malenka +1 more
TL;DR: A new form of synaptic plasticity, homosynaptic long-term depression (LTD) has also recently been documented, which, like LTP, requires Ca2+ entry through the NMDA receptor, and current work suggests that this LTD is a reversal ofLTP, and that the mechanisms of LTP and LTD may converge at the level of specific phosphoproteins.
References
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Journal ArticleDOI
A requirement for the intercellular messenger nitric oxide in long-term potentiation
TL;DR: Findings suggest that nitric oxide liberated from postsynaptic neurons may travel back to presynaptic terminals to cause LTP expression.
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Intracellular injections of EGTA block induction of hippocampal long-term potentiation
TL;DR: It is reported that intracellular injections of the calcium chelator EGTA block the development of LTP and this results strongly suggest that LTP is caused by a modification of the postsynaptic neurone and that its induction depends on the level of free calcium.
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Tests of the roles of two diffusible substances in long-term potentiation: evidence for nitric oxide as a possible early retrograde messenger.
TL;DR: Two major membrane-permeant candidate retrograde messengers are investigated, arachidonic acid and nitric oxide, and no enhances spontaneous presynaptic release of transmitter from hippocampal neurons in dissociated cell culture, suggesting that NO might be a retrograde messenger in LTP.
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Postsynaptic calcium is sufficient for potentiation of hippocampal synaptic transmission
TL;DR: It is demonstrated that an increase in postsynaptic calcium is necessary to induce LTP and sufficient to potentiate synaptic transmission.
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Possible involvement of nitric oxide in long-term potentiation.
TL;DR: It is reported here that the NO-synthase inhibitor, L-N omega-nitro-arginine, blocks LTP and that sodium nitroprusside, which releases NO, produces a long-lasting enhancement in synaptic efficacy which is not additive with tetanus-induced LTP.