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BIO254:Silent: Difference between revisions
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NMDA receptors are actively inhibited by APV, which can thereby regulate '''silent synapse''' activity. | NMDA receptors are actively inhibited by APV, which can thereby regulate '''silent synapse''' activity. | ||
==Long-term potentiation (LTP)== | ==Long-term potentiation (LTP)== | ||
[[BIO254:LTP|Long-term potentiation]] (LTP) describes the process | [[BIO254:LTP|Long-term potentiation]] (LTP) describes the process whereby 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 the postsynaptic depolarization threshold that must be exceeded in order to induce LTP. The voltage dependency of the NMDA receptor (NMDAR) establishes this threshold. | * '''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 the NMDA receptor (NMDAR) establishes this threshold. | ||
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Unlike CA3-CA1 LTP, mossy fiber LTP is not dependent on NMDAR, and might be expressed primarily by increased presynaptic neurotransmitter release. | Unlike CA3-CA1 LTP, mossy fiber LTP is not dependent on NMDAR, and might be expressed primarily by increased presynaptic neurotransmitter release. | ||
==Molecular Mechanisms Underlying LTP== | |||
Although LTP was discovered more than three decades ago, the molecular mechanisms contributing to this phenomenon are still not well understood. The properties of NMDA-type glutamate receptors were first elucidated in the mid-1980s, and at about the same time, neurobiologists found that antagonists (inhibitors) of NMDA receptors actually prevented LTP. The "AND" characteristics of NMDA receptors contribute to both the specificity and associativity of LTP. For example, when only one group of synaptic inputs is strongly stimulated, LTP is confined to the active synapses (selectivity), since glutamate opens NMDA receptors only at the stimulated sites. However, in terms of associativity, applying a weakly stimulating input current releases glutamate but cannot depolarize the post-synaptic terminal enough to relieve the Mg++ block. When neighboring stimulations are applied to a weak input, these currents work "associatively" to both depolarize and unblock the NMDA receptors on the cell dendrite. | |||
==<h3>Recent updates to the site</h3>== | ==<h3>Recent updates to the site</h3>== | ||
{{Special:Recentchanges/BIO254&limit=50}} | {{Special:Recentchanges/BIO254&limit=50}} | ||
</div> | </div> | ||
