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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.
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.
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 ...
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 ...
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.
Long-term potentiation (LTP) is one mechanism where repeated EPSPs occur, strengthening neural circuits involved in learning, allowing the brain to store information more effectively. Long-term depression (LTD) is another mechanism where IPSPs occur weakening less-used synapses, refining learning by filtering out unnecessary information.
Large postsynaptic calcium transients are known to trigger synaptic potentiation (long-term potentiation). The mechanism for spike-timing-dependent depression is less well understood, but often involves either postsynaptic voltage-dependent calcium entry/mGluR activation, or retrograde endocannabinoids and presynaptic NMDARs. [12]
The research indicates that this long term potentiation or in the case of inhibitory synapses, long term depression of the synapse occurs after prolonged stimulation of two neurons at the same time. Long term potentiation is known to have a role in memory and learning, which could be useful in treating diseases like Alzheimers.