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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.
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.
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.
The theory was validated in part by the discovery of long-term potentiation. Studies of LTP on multiple presynaptic cells stimulating a postsynaptic cell uncovered the property of associativity. A weak neuronal stimulation onto a pyramidal neuron may not induce long-term potentiation.
Long-term depression (LTD) and long-term potentiation (LTP) are two forms of long-term plasticity, lasting minutes or more, that occur at excitatory synapses. [2] NMDA-dependent LTD and LTP have been extensively researched, and are found to require the binding of glutamate, and glycine or D-serine for activation of NMDA receptors. [24]
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 ...
For example, when plastic changes lead to long-term depression, calcineurin is used. Conversely, when plasticity leads to long-term potentiation, CaMKII is used. [ 5 ] In order for synaptic plasticity to be input-specific, these synaptic tags are essential on post-synaptic targets, to ensure synaptic potentiation is localized. [ 5 ]