Neurophysiology: memory and long-term potentiation: practice question

A Physiology question in the style of the NEET PG paper. Answer it first, then read why the right option is right and why each of the others is wrong.

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Physiology · Neurophysiology: memory and long-term potentiation

Sample item

A patient with bilateral hippocampal damage after herpes encephalitis cannot form new declarative memories. Which cellular event underlies hippocampal long-term potentiation?

Original practice item, not a recalled exam question. Nothing here is recorded.

The answer and the reasoning

D. Coincident glutamate release and postsynaptic depolarisation that removes the magnesium block of NMDA receptors, allowing calcium entry

Long-term potentiation needs glutamate binding and depolarisation from AMPA receptor currents, which expels Mg2+ from the NMDA channel. Calcium entry activates kinases that insert more AMPA receptors, strengthening the synapse and supporting consolidation of memory.

Option by option

  • A. Reuptake of glutamate by astrocytes that lowers synaptic strength

    Glutamate reuptake terminates transmission and does not underlie potentiation.

  • B. Opening of voltage-gated sodium channels at the axon terminal alone

    Presynaptic sodium channel opening alone does not strengthen the synapse.

  • C. Presynaptic GABA release that hyperpolarises the postsynaptic cell

    GABA mediates inhibition and does not potentiate synapses.

  • D. Coincident glutamate release and postsynaptic depolarisation that removes the magnesium block of NMDA receptors, allowing calcium entry (correct)

    Correct. Calcium influx through NMDA receptors triggers strengthening of the synapse.

Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.

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Questions about this Physiology question

What is the answer to this Physiology question?

The best answer is D, Coincident glutamate release and postsynaptic depolarisation that removes the magnesium block of NMDA receptors, allowing calcium entry. Long-term potentiation needs glutamate binding and depolarisation from AMPA receptor currents, which expels Mg2+ from the NMDA channel.

Why is "Reuptake of glutamate by astrocytes that lowers synaptic strength" not the answer?

Glutamate reuptake terminates transmission and does not underlie potentiation.

Why is "Opening of voltage-gated sodium channels at the axon terminal alone" not the answer?

Presynaptic sodium channel opening alone does not strengthen the synapse.

Why is "Presynaptic GABA release that hyperpolarises the postsynaptic cell" not the answer?

GABA mediates inhibition and does not potentiate synapses.

What concept does this question test?

It tests Neurophysiology: memory and long-term potentiation in Physiology. Calcium entry activates kinases that insert more AMPA receptors, strengthening the synapse and supporting consolidation of memory.

How hard is this question?

We tag it as an application question: it asks you to use a fact on a patient or a finding. The tag is our own editorial judgement, not an official difficulty rating, so read the reason for every option, not only the answer.

How should I study Neurophysiology: memory and long-term potentiation?

For each system, sketch the key graph (pressure–volume loop, oxygen dissociation curve, nephron handling) and explain it aloud. Then use the flashcards and the other Physiology questions on this site to test what stuck.

Is this a real NEET PG question?

No. It is an original practice item (editorial status: sample, version 1). NextPrep does not publish recalled or leaked questions, and independent faculty review of this item has not been completed yet, so confirm important facts in a standard textbook.