Long-term potentiation (LTP) at hippocampal CA3-CA1 synapses is critical for memory formation. The initial requirement for NMDA receptor activation during LTP induction depends on which co-requirement?
- A Presynaptic vesicle release of glycine to co-activate NMDA receptors in place of glutamate
- B Retrograde NO signaling from the postsynaptic cell enhancing presynaptic glutamate release first
- C Simultaneous postsynaptic depolarization sufficient to relieve Mg2+ block of NMDA receptor channels, allowing Ca2+ influx ✓
- D mGluR activation leading to IP3-mediated intracellular Ca2+ release that then opens NMDA receptors
Explanation
NMDA receptors are coincidence detectors: they require simultaneous glutamate binding AND postsynaptic depolarization. At resting membrane potential, the NMDA receptor channel pore is physically blocked by Mg2+ ions. Only when the postsynaptic membrane is sufficiently depolarized (typically by concurrent AMPA receptor activation from strong stimulation) is Mg2+ expelled from the channel, allowing Ca2+ influx. This Ca2+ influx activates CaMKII and other kinases, which phosphorylate AMPA receptors and promote their insertion into the synapse, increasing synaptic strength — the synaptic basis of Hebbian learning.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.