During NMDA receptor–mediated signaling, which ion's influx is critical for triggering synaptic strengthening?

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Multiple Choice

During NMDA receptor–mediated signaling, which ion's influx is critical for triggering synaptic strengthening?

Explanation:
Calcium influx through NMDA receptors is the key signal that triggers synaptic strengthening. NMDA channels open only when glutamate is bound and the postsynaptic cell is depolarized, relieving an Mg2+ block. Once open, Ca2+ enters the cell and activates calcium-dependent signaling cascades (such as CaMKII and other kinases) that promote AMPA receptor trafficking to the synapse and initiate gene transcription changes, producing long-term potentiation. While Na+ can also pass through NMDA receptors, it is the rise in intracellular Ca2+ that drives the enhancement of synaptic strength. Potassium and chloride ions are not the primary drivers of this NMDA-mediated plasticity.

Calcium influx through NMDA receptors is the key signal that triggers synaptic strengthening. NMDA channels open only when glutamate is bound and the postsynaptic cell is depolarized, relieving an Mg2+ block. Once open, Ca2+ enters the cell and activates calcium-dependent signaling cascades (such as CaMKII and other kinases) that promote AMPA receptor trafficking to the synapse and initiate gene transcription changes, producing long-term potentiation. While Na+ can also pass through NMDA receptors, it is the rise in intracellular Ca2+ that drives the enhancement of synaptic strength. Potassium and chloride ions are not the primary drivers of this NMDA-mediated plasticity.

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