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BIO254:Silent: Difference between revisions
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[[BIO254:LTP|Long-term potentiation]] (LTP) describes the process wherein the synaptic efficacy of two neurons is strengthened over time, in a way that depends on the simultaneity of firing (spike timing dependent plasticity). The best-studied form of this is hippocampal CA3-CA1 LTP, demonstrated by Timothy Bliss and Terje Lomo (1973). Brief high-frequency (tetanic) stimulation of a presynaptic cell can result in long-term enhancement of synaptic transmission. LTP additionally exhibits the following properties: | [[BIO254:LTP|Long-term potentiation]] (LTP) describes the process wherein the synaptic efficacy of two neurons is strengthened over time, in a way that depends on the simultaneity of firing (spike timing dependent plasticity). The best-studied form of this is hippocampal CA3-CA1 LTP, demonstrated by Timothy Bliss and Terje Lomo (1973). Brief high-frequency (tetanic) stimulation of a presynaptic cell can result in long-term enhancement of synaptic transmission. LTP additionally exhibits the following properties: | ||
* '''Cooperativity''': The probability of inducing LTP increases with the number of stimulated afferents, and the strength of their stimulation. This reflects | * '''Cooperativity''': The probability of inducing LTP increases with the number of stimulated afferents, and the strength of their stimulation. This reflects the postsynaptic depolarization threshold that must be exceeded in order to induce LTP. The voltage dependency of NMDAR establishes this threshold. | ||
* '''Input specificity''': LTP is restricted to the synapses that triggered the process, and does not propagate to nearby synapses. | * '''Input specificity''': LTP is restricted to the synapses that triggered the process, and does not propagate to nearby synapses. | ||
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It was found that CA3-CA1 LTP requires both NMDAR and Ca<sup>2+</sup>, and involves depolarization of the postsynaptic cell, activation of NMDA receptors in that cell, the resulting influx of Ca<sup>2+</sup>, and the activation of secondary messengers by Ca<sup>2+</sup>. | It was found that CA3-CA1 LTP requires both NMDAR and Ca<sup>2+</sup>, and involves depolarization of the postsynaptic cell, activation of NMDA receptors in that cell, the resulting influx of Ca<sup>2+</sup>, and the activation of secondary messengers by Ca<sup>2+</sup>. | ||
The specific expression mechanisms of CA3-CA1 LTP are highly controversial. However, we do know that the expression of LTP is likely to involve both pre- and postsynaptic mechanisms, and that the probability of presynaptic neurotransmitter release is increased after LTP induction. At the postsynaptic cell, AMPA receptors are inserted into the cell membrane, which increases the conductance of the AMPA channel and thereby converts silent synapses into functional ones. | The specific expression mechanisms of CA3-CA1 LTP are highly controversial. However, we do know that the expression of LTP is likely to involve both pre- and postsynaptic mechanisms, and that the probability of presynaptic neurotransmitter release is increased after LTP induction. At the postsynaptic cell, AMPA receptors are inserted into the cell membrane, which increases the conductance of the AMPA channel and thereby converts '''silent synapses''' into functional ones. | ||
After the early phase of LTP (E-LTP) in which these pre- and post-synaptic changes occur, the late phase (L-LTP) can lead to the formation of new synapses. | After the early phase of LTP (E-LTP) in which these pre- and post-synaptic changes occur, the late phase (L-LTP) can lead to the formation of new synapses. | ||
