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They are important for Long-term potentiation, learning and memory.
The theory was validated in part by the discovery of long-term potentiation.
This process of synaptic strengthening is known as long-term potentiation.
These skills would not come until the later half of the 20th century, at about the same time as the discovery of long-term potentiation.
Long-term potentiation in particular gets its name from the length of time which the increased synaptic strength remains.
These two drugs also work together to induce long-term potentiation in neuronal populations.
But the problem was that long-term potentiation takes place in the pyramidal cells of the hippocampus.
CREB is necessary for the late stage of long-term potentiation.
Long-term potentiation is the persistent increase in the strength of a chemical synapse that lasts from hours to days.
The mechanism for this action is thought to be through promoting the induction of long-term potentiation between synapses in the brain.
This pathway specifically affects cortical migration and long-term potentiation.
It is associated with long-term potentiation.
Retrograde signaling may also play a role in long-term potentiation, a proposed mechanism of learning and memory, although this is controversial.
Another mechanism for input-specific long-term potentiation is temporal.
He immediately saw that it might provide a clue to long-term potentiation, the mechanism by which long-term memories are stored.
The best understood form of long-term potentiation is induced by the activation of the receptor complex.
They called the phenomenon long-term potentiation, soon abbreviated to LTP.
Forms of long-term plasticity include long-term depression and long-term potentiation.
Long-term potentiation is only propagated to those synapses according to the rules of associativity and cooperativity.
A weak neuronal stimulation onto a pyramidal neuron may not induce long-term potentiation.
A phenomenon called long-term potentiation allows a synapse to increase strength with increasing numbers of transmitted signals between the two neurons.
Specifically, glutamate is involved in long-term potentiation, which is thought to be one of the main mechanisms that underlies learning and memory.
It modulates synaptic plasticity by enhancing the induction and maintenance of long-term potentiation.
To his delight, it prevented long-term potentiation, evidence that carbon monoxide was likely to be the long-sought signaling substance.
Also, fear conditioning, a type of memory that is impaired following amygdala damage, is mediated in part by long-term potentiation.
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