Scientific Understanding of Consciousness
Consciousness as an Emergent Property of Thalamocortical Activity

Long-Term Potentiation

 

 

Long-term potentiation (LTP) is a mechanism for long-lasting facilitation of synaptic transmission; a permanent increase in synaptic efficacy, resulting from repeated activation of a presynaptic neuron and its firing the postsynaptic neuron. (Eichenbaum; Neuroscience of Memory, 346)

Long-term potentiation (LTP), the mechanism by which memories are formed in synapses. (Andreasen; Creating Brain, 60)

Long-term potentiation (LTP) can last for many hours or even days. (Kandel; Principles of Neural Science, 275)

LTP has phases. Early LTP lasts 1-3 hours; does not require protein synthesis. (Kandel; Principles of Neural Science, 1262)

A more persistent phase of the LTP (called late LTP) that lasts for at least 24 hours and requires new protein and RNA synthesis. (Kandel; Principles of Neural Science, 1262)

Late phase LTP involves the activation, perhaps the growth, of additional presynaptic machinery for transmitter release and the insertion of new clusters of postsynaptic receptors. (Kandel; Principles of Neural Science, 1264)

 

Research Study Strengthening Synaptic Connections by NMDA for Long-Term Potentiation (LTP)

Research Study Dendritic Spines Dispersed Signals Integrated in Nuclear ERK

 

The discovery of what has come to be known as long term potentiation (LTP) emerged from experiments that Per Andersen and Lomo, then a PhD student, were conducting at the University of Oslo during the mid-1960s on the phenomenon of frequency potentiation in excitatory hippocampal pathways. (Andersen; Hippocampus Book, 344)

During the period from 1966 to mid-1980s, the major characteristics of LTP, including its persistence, and specificity, and associativity, were established, the critical role of the NMDA receptor in the induction of LTP identified, and the first steps taken to link LTP to hippocampus dependent learning. (Andersen; Hippocampus Book, 343)

Although long term potentiation was first described in the dentate gyrus, most of the studies in the decades that followed in its original description have focused on the CA1 region. (Andersen; Hippocampus Book, 133)

LTP takes a very different form at the largest synapses in the hippocampus, indeed among the largest in the mammalian brain -- the synapses made by granule cell axons (the mossy fibers) on CA3 pyramidal cells. (Andersen; Hippocampus Book, 398)

 

The synaptic plasticity of long term potentiation and depression, LTP and LTD, persist for hours if not longer. (Andersen; Hippocampus Book, 210)

Dopamine has been shown to have a role in synaptic plasticity within the striatum, being implicated in both long term potentiation (LTP) and long-term depression (LTD). (Alexander; Basal Ganglia, 142)

With their combined voltage dependency and ligand specificity, NMDA receptors are widely assumed to play a role in at least one form of activity-dependent synaptic plasticity, i.e. LTP. (Alexander; Basal Ganglia, 142)

NMDA Receptors and LTP

Only temporally overlapping pairing of two inputs produce associative LTP. (Brown; Hebbian Plasticity, 455)

The form of LTP that has been most extensively studied is the variety that occurs in the Schaffer collateral synaptic input to the pyramidal neurons of hippocampal region CA1. (Brown; Hebbian Plasticity, 455)

The induction of the most commonly studied form of LTP at the Schaffer collateral synapses is controlled by the NMDA subclass of glutamate receptor. (Brown; Hebbian Plasticity, 456)

The common working hypothesis is that the Ca2+ influx through the NMDA receptor-gated channel and the resultant increase in postsynaptic Ca2+ are partly responsible for triggering the induction of LTP. (Brown; Hebbian Plasticity, 456)

The influx of Ca2+ ions through NMDA receptor channels triggers a cascade of molecular processes that leads to various forms of synaptic plasticity, including short-term potentiation (STP), long term potentiation (LTP), and long term depression. (Liaw; NMDA Receptors, 644)

The three unique properties NMDA receptors (i.e. slow conductance, voltage and transmitter dependency, and calcium permeability) provide the basis for their involvement in STP, LTP, synaptic integration, motor pattern generation, and epileptiform activity. (Liaw; NMDA Receptors, 647)

Spines are of considerable interest as sites for activity-dependent mechanisms, such as long term potentiation (LTP), that may underlie learning. (Wilson; Olfactory Cortex, 671)

Both the afferent excitatory inputs and the recurrent excitatory inputs are made onto the spines, and both show properties of LTP. (Wilson; Olfactory Cortex, 671)

 

 

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