Studies: One contemporary study on schizophrenia — Edexcel A-Level Psychology
Test yourself on Studies: One contemporary study on schizophrenia with PEARSON EDEXCEL A-Level practice questions.
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Studies: One contemporary study on schizophrenia explained
A review rather than a new experiment, this paper argues that excess dopamine in the striatum cannot be the whole account of psychosis, because drugs that block the NMDA glutamate receptor, phencyclidine and ketamine among them, produce positive symptoms, negative symptoms and cognitive disturbance in healthy volunteers, and it is exactly the negative and cognitive symptoms that antipsychotics leave untouched. Drawing on work with mice depleted of monoamines, the authors map the loops running from cortex to striatum to thalamus and back, in which glutamate can open or close the thalamic filter that shields the cortex from sensory flooding while dopamine acts as the brake. Psychosis can therefore arise with or without too much dopamine, which predicts different drug targets for different patients.
Your focus
- 5.3.2 Carlsson et al. (2000) Network interactions in schizophrenia – therapeutic implications.
Studies: One contemporary study on schizophrenia exam tips
Marking Points
- State the aim and the kind of evidence: the paper re-examines the dopamine hypothesis and builds a glutamate based account with therapeutic implications, and it does so by reviewing animal and human pharmacological work rather than by testing a sample, so it has no participants, no conditions and no statistics of its own.
- Give the pharmacological evidence: antagonists at the NMDA receptor reproduce the whole symptom picture in people who are not ill, which a purely dopamine based model cannot explain, and low activity at those receptors is what the authors mean by hypoglutamatergia.
- Explain the circuit rather than listing chemicals: cortical glutamate pathways influence the thalamic filter both directly and by way of the striatum and pallidum, dopamine opposes them, and it is the balance between the two, not the level of either alone, that decides whether the cortex is flooded.
- Set out the therapeutic implications the title promises: different patients may need different targets, including agents that stabilise dopamine rather than block it wholesale and drugs acting on glutamate, which offers a route to the negative symptoms that standard antipsychotics barely touch.
- Evaluate in both directions: converging evidence from several species and several drugs is a genuine strength and the applied payoff is real, but a review selects its evidence, mouse behaviour is a thin model of human thought, and the account is reductionist and biologically determinist.
Examiner Tips
- 💡It is the prescribed contemporary study for schizophrenia, so it is most often examined beside the classic study, and compare questions reward a planned contrast on method, sample, level of explanation and determinism.
- 💡For a methodological evaluation of a review, write about breadth and convergence as strengths and about selection of sources, extrapolation from animals and the absence of new data as weaknesses.
- 💡In an essay on explanations of schizophrenia, use it as evaluation of the dopamine hypothesis rather than describing it at length, because the description marks there are for the explanation, not for the study.
- 💡Learn one sentence on why the study matters for treatment, since usefulness questions in the applications paper reward an applied consequence.
Common Mistakes
- Describing it as an experiment with a sample and a procedure. If a question asks about sampling or design, the correct answer explains that this is a review of existing animal and pharmacological studies, which is itself a methodological point worth marks.
- Saying that glutamate replaces dopamine. The argument is interaction and imbalance across a circuit, with dopamine still central to the model.
- Confusing hypoglutamatergia with too much glutamate. The proposal is reduced transmission at the NMDA receptor, which is why blocking that receptor mimics the disorder.
- Using ketamine studies to claim that recreational drugs cause lasting schizophrenia, when what the evidence shows is a short term model of the symptoms.
- Writing a general essay on the dopamine hypothesis and never naming anything from this paper, which loses every mark tied to the named study.