Final Answer:
The induction of long-term potentiation in the hippocampus would be blocked by option d. a drug such as AP5 that blocks NMDA receptors.
Step-by-step explanation:
Long-term potentiation (LTP) is a synaptic phenomenon associated with persistent strengthening of the communication between neurons, particularly in the hippocampus, a crucial region for learning and memory. NMDA receptors play a pivotal role in the induction of LTP. The activation of NMDA receptors is contingent upon the binding of glutamate and the simultaneous depolarization of the postsynaptic membrane.
This depolarization allows magnesium ions (Mg^2+) to exit the NMDA receptor channel, unblocking it and permitting calcium ions (Ca^2+) influx. The elevation of intracellular calcium is a key step in initiating the molecular processes underlying LTP.
Option d, which involves using a drug like AP5 that blocks NMDA receptors, would impede the normal functioning of these receptors. AP5 is a competitive antagonist that competes with glutamate for binding sites on the NMDA receptor. By blocking NMDA receptors, AP5 prevents the influx of calcium ions into the postsynaptic cell, disrupting the cascade of events required for the induction of LTP. Therefore, the administration of AP5 would hinder the synaptic plasticity associated with long-term potentiation in the hippocampus.
In contrast, the other options (a, b, c, e) are not likely to block the induction of LTP. Infusing glutamate (option a) or using high-frequency electrical pulses (option b) would normally facilitate LTP induction. Option c, a drug that activates NMDA receptors, would enhance rather than block LTP. Option e, injecting a drug that activates calcium ions in the postsynaptic cell, does not specifically target the NMDA receptor and may not interfere with the required events for LTP induction.