Neurophysiology: glutamate excitotoxicity: 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: glutamate excitotoxicity

Sample item

In the penumbra around a cerebral infarct, extracellular glutamate remains high and neurones die despite partial blood flow. Which sequence explains the neuronal death?

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

The answer and the reasoning

A. NMDA overactivation with calcium overload

Failure of energy-dependent glutamate uptake leaves glutamate high, which overactivates NMDA receptors and allows massive calcium entry. Calcium activates proteases, lipases and nucleases and generates free radicals, killing the neurone.

Option by option

  • A. NMDA overactivation with calcium overload (correct)

    Correct. Glutamate-mediated calcium overload is the excitotoxic pathway.

  • B. Excess GABA release causing silence

    GABA is an inhibitory transmitter and its excess is not the cause of injury here.

  • C. Loss of sodium-potassium pump from excess potassium entry

    Pump failure is a result of energy loss and not the specific glutamate-driven mechanism.

  • D. Opening of chloride channels causing hyperpolarisation

    Chloride-mediated hyperpolarisation is inhibitory, not toxic.

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 A, NMDA overactivation with calcium overload. Failure of energy-dependent glutamate uptake leaves glutamate high, which overactivates NMDA receptors and allows massive calcium entry.

Why is "Excess GABA release causing silence" not the answer?

GABA is an inhibitory transmitter and its excess is not the cause of injury here.

Why is "Loss of sodium-potassium pump from excess potassium entry" not the answer?

Pump failure is a result of energy loss and not the specific glutamate-driven mechanism.

Why is "Opening of chloride channels causing hyperpolarisation" not the answer?

Chloride-mediated hyperpolarisation is inhibitory, not toxic.

What concept does this question test?

It tests Neurophysiology: glutamate excitotoxicity in Physiology. Calcium activates proteases, lipases and nucleases and generates free radicals, killing the neurone.

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: glutamate excitotoxicity?

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.