Long-term potentiation (LTP) at hippocampal CA3-CA1 synapses requires coincident presynaptic and postsynaptic activity. The molecular switch that detects this coincidence is:

• A NMDA receptor — requires both glutamate binding and postsynaptic depolarisation to relieve the Mg2+ block, allowing Ca2+ influx that triggers LTP induction ✓
• B AMPA receptor — repeated activation causes phosphorylation-dependent insertion of additional AMPA receptors into the synapse
• C mGluR1/5 — activation by glutamate releases IP3, leading to ER Ca2+ release and CaMKII activation
• D Voltage-gated L-type Ca2+ channels in the dendritic spine, activated by postsynaptic depolarisation alone

Explanation

The NMDA (N-methyl-D-aspartate) receptor is the molecular coincidence detector for LTP induction. At resting membrane potential, the NMDA receptor channel pore is blocked by Mg2+ ions. For Mg2+ unblocking, the postsynaptic membrane must be sufficiently depolarised (by AMPA receptor activation during repeated stimulation). When both conditions are met — glutamate binding (ligand gate) AND postsynaptic depolarisation (removes Mg2+ block) — Ca2+ flows into the dendritic spine through the NMDA receptor. The resulting Ca2+ transient activates CaMKII (calcium-calmodulin kinase II) and other signalling cascades that phosphorylate existing AMPA receptors (increasing conductance) and insert additional AMPA receptors into the synapse, increasing synaptic efficacy. AMPA receptor insertion (option B) is the expression mechanism of LTP, not the induction trigger. Options C and D contribute to some forms of synaptic plasticity but are not the primary coincidence detector.

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

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