long-term potentiation

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long-term potentiation

n.
Repeated presynaptic stimulation of a nerve, either naturally or in vitro, that results in the long-lasting increased strength of a synapse and is thought to be necessary for learning and memory formation.
American Heritage® Dictionary of the English Language, Fifth Edition. Copyright © 2016 by Houghton Mifflin Harcourt Publishing Company. Published by Houghton Mifflin Harcourt Publishing Company. All rights reserved.
References in periodicals archive
Long-term potentiation (LTP) and long-term depression (LTD) refer to lasting increases and decreases in synaptic efficacy that are produced by selective patterns of input activity.
Effects of saffron extract and its constituent crocin on learning behaviour and long-term potentiation. Phytother Res.
Keywords: Eugenol; Glutamate mediated synaptic transmission; Hippocampal slices; Long-term potentiation
Inhibition of 14-3-3 proteins in the hippocampus impairs associative learning and memory behaviors and suppresses long-term potentiation (LTP) at hippocampal CA3-CA1 synapses of the 14-3-3 FKO mice [41].
Long-term potentiation strengthens the connection between two neurons, and seems to be important for memory and learning.
Nitric oxide acts directly in the presynaptic neuron to produce long-term potentiation in cultured hippocampal neurons.
(1992, 1996, 1998, 1999) as a central mechanism in MCS, and such neural sensitization is produced by the process of long-term potentiation (LTP).
Since the discovery of long-term potentiation (LTP) (Bliss and Lomo, 1973; Bliss and Collingridge, 1993) and distinct characteristics of NMDA receptors, NMDA-receptor-dependent LTP has been prominently regarded as a mechanism to explain cellular events underlying associative learning and memory acquisition (Bliss and Lomo, 1973; Bliss and Collingridge, 1993; Tsien et al., 1996; Kiyama et al., 1998; Martin and Morris, 2002).
Rather, hippocampal cells fail to mature normally, causing a reduction in long-term potentiation, or the cellular basis of how the brain learns.
One of those mechanisms is thought to rely in an optimal adjustment of the strength of communication between neurons through long-term potentiation, by which that strength increases, and long-term depression, by which some of these connections weaken.
CaMKII, a serine/threonine kinase activated during long-term potentiation via the influx of [Ca.sup.2+] through the NMDARs, is likely of prime importance in terms of linking transient calcium signals to neuronal plasticity (38).
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