Long-term potentiation (LTP) at hippocampal Schaffer collateral–CA1 synapses requires NMDA receptor activation and subsequent CaMKII autophosphorylation. CaMKII phosphorylates AMPA receptor subunit GluA1 at Ser831 and drives AMPA receptor insertion. Which aspect of this mechanism is responsible for 'silent synapses' becoming active during LTP?

• A Silent synapses lack functional NMDA receptors; LTP inserts de novo NMDA receptors to enable activation
• B Silent synapses have low neurotransmitter release probability; LTP increases vesicle docking proteins presynaptically
• C Silent synapses lack presynaptic vesicles; LTP induces anterograde axonal transport of new vesicles
• D Silent synapses contain NMDA receptors but lack AMPA receptors; LTP-driven AMPA receptor insertion converts them to active synapses ✓

Explanation

Silent synapses are morphologically intact synapses that contain NMDA receptors but lack AMPA receptors in the postsynaptic density. At resting membrane potential, NMDA receptors are Mg²⁺-blocked and produce no current, making the synapse physiologically silent to normal synaptic transmission. During LTP induction, strong depolarization (via already-active synapses) relieves the Mg²⁺ block, NMDA receptors open, Ca²⁺ influx activates CaMKII, which phosphorylates GluA1 and recruits AMPA receptors from internal recycling endosomes to the synaptic membrane — 'awakening' the silent synapse. This is a key postsynaptic mechanism of LTP expression.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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