Schizophrenia: glutamate hypothesis: practice question

A Psychiatry 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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Psychiatry · Schizophrenia: glutamate hypothesis

Sample item

Phencyclidine and ketamine produce positive, negative and cognitive symptoms that resemble schizophrenia. This supports which hypothesis?

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

The answer and the reasoning

B. Hypofunction of NMDA glutamate receptors

NMDA receptor antagonists such as PCP and ketamine reproduce the full range of schizophrenic symptoms in healthy people, including negative and cognitive features. This led to the glutamate hypofunction hypothesis, complementing the dopamine hypothesis. It also underlies research on glycine and D-serine augmentation.

Option by option

  • A. Deficiency of histamine in the hypothalamus

    Histamine deficiency is not a recognised cause of schizophrenia.

  • B. Hypofunction of NMDA glutamate receptors (correct)

    Correct. Blocking NMDA receptors mimics schizophrenia, suggesting NMDA hypofunction.

  • C. Excess acetylcholine in the basal forebrain

    Cholinergic excess is not the basis of this observation.

  • D. Hyperfunction of GABA receptors

    GABA hyperfunction is not implicated; reduced GABA interneuron function is the proposed finding.

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 Psychiatry question

What is the answer to this Psychiatry question?

The best answer is B, Hypofunction of NMDA glutamate receptors. NMDA receptor antagonists such as PCP and ketamine reproduce the full range of schizophrenic symptoms in healthy people, including negative and cognitive features.

Why is "Deficiency of histamine in the hypothalamus" not the answer?

Histamine deficiency is not a recognised cause of schizophrenia.

Why is "Excess acetylcholine in the basal forebrain" not the answer?

Cholinergic excess is not the basis of this observation.

Why is "Hyperfunction of GABA receptors" not the answer?

GABA hyperfunction is not implicated; reduced GABA interneuron function is the proposed finding.

What concept does this question test?

It tests Schizophrenia: glutamate hypothesis in Psychiatry. This led to the glutamate hypofunction hypothesis, complementing the dopamine hypothesis. It also underlies research on glycine and D-serine augmentation.

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 Schizophrenia: glutamate hypothesis?

Learn each diagnosis by its core features and its first-line treatment. Then use the flashcards and the other Psychiatry 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.