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Memory consolidation was first referred to in the writings of the renowned Roman teacher of rhetoric Quintillian.He noted the "curious fact... that the interval of a single night will greatly increase the strength of the memory," and presented the possibility that "... the power of recollection .. undergoes a process of ripening and maturing during the time which intervenes."
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 ...
Synaptic allocation pertains to mechanisms that influence how synapses come to store a given memory. [3] Intrinsic to the idea of synaptic allocation is the concept that multiple synapses can be activated by a given set of inputs, but specific mechanisms determine which synapses actually go on the encode the memory.
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.
Chemical synaptic transmission is the transfer of neurotransmitters or neuropeptides from a presynaptic axon to a postsynaptic dendrite. [3] Unlike an electrical synapse, the chemical synapses are separated by a space called the synaptic cleft, typically measured between 15 and 25 nm. Transmission of an excitatory signal involves several steps ...
Calcium enters the axon terminal during an action potential, causing release of the neurotransmitter into the synaptic cleft. After its release, the transmitter binds to and activates a receptor in the postsynaptic membrane. Deactivation of the neurotransmitter.
Neuronal activity triggers an increase in astrocytic calcium levels, prompting the release of gliotransmitters, such as glutamate, ATP, and D-serine.These gliotransmitters diffuse into the extracellular space, interacting with nearby neurons and influencing synaptic transmission. By regulating extracellular neurotransmitter levels, astrocytes ...