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Long-term potentiation (LTP) is a persistent increase in synaptic strength following high-frequency stimulation of a chemical synapse. Studies of LTP are often carried out in slices of the hippocampus, an important organ for learning and memory. In such studies, electrical recordings are made from cells and plotted in a graph such as this one.
Much of the work on long-lasting synaptic changes between vertebrate neurons (such as long-term potentiation) involves the use of non-physiological experimental stimulation of brain cells. However, some of the physiologically relevant synapse modification mechanisms that have been studied in vertebrate brains do seem to be examples of Hebbian ...
Early long-term potentiation (E-LTP) is the first phase of long-term potentiation (LTP), a well-studied form of synaptic plasticity, and consists of an increase in synaptic strength. [1] LTP could be produced by repetitive stimulation of the presynaptic terminals, and it is believed to play a role in memory function in the hippocampus, amygdala ...
The induction of NMDA receptor-dependent long-term potentiation (LTP) in chemical synapses in the brain occurs via a fairly straightforward mechanism. [1] [2] A substantial and rapid rise in calcium ion concentration inside the postsynaptic cell (or more specifically, within the dendritic spine) is most possibly all that is required to induce LTP.
Metaplasticity is a term originally coined by W.C. Abraham and M.F. Bear to refer to the plasticity of synaptic plasticity. [1] Until that time synaptic plasticity had referred to the plastic nature of individual synapses. However this new form referred to the plasticity of the plasticity itself, thus the term meta-plasticity. The idea is that ...
Of the estimated 30-40 genes that comprise the total neuronal IEG response, all are prototypical activity-dependent genes and a number have been implicated in learning and memory. For example, zif268, Arc, beta-activin, tPA, Homer, and COX-2 have all been implicated in long-term potentiation (LTP), [25] a cellular correlate of learning and memory.
Two molecular mechanisms for synaptic plasticity involve the NMDA and AMPA glutamate receptors. Opening of NMDA channels (which relates to the level of cellular depolarization) leads to a rise in post-synaptic Ca 2+ concentration and this has been linked to long-term potentiation, LTP (as well as to protein kinase activation); strong depolarization of the post-synaptic cell completely ...
Neural plasticity is the neuronal basis for changes in how the mind works, including learning, the formation of memory, and changes in intelligence. One well-studied form of plasticity is Long-Term Potentiation (LTP). [6] It refers to a change in neural connectivity as a result of high activation on both sides of a synaptic cleft.