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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.
Long-term potentiation (neurophysiology), a long-lasting enhancement in signal transmission between neurons 'The All-Species Living Tree' Project , a project to create a phylogeny of all Bacteria and Archaea
According to the BCM model, when a pre-synaptic neuron fires, the post-synaptic neurons will tend to undergo LTP if it is in a high-activity state (e.g., is firing at high frequency, and/or has high internal calcium concentrations), or LTD if it is in a lower-activity state (e.g., firing in low frequency, low internal calcium concentrations). [1]
Hebb described an early concept of the theory, not the actual mechanics themselves. Hebbian plasticity involves two mechanisms: LTP and LTD, discovered by Bliss and Lomo in 1973. LTP, or long-term potentiation, is the increase of synapse sensitivity due to a prolonged period of activity in both the presynaptic and postsynaptic neuron. This ...
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.
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 ...
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]