Skip to content

Course home

Sign up

3.2.6 Schizophrenia research study: Daniel et al. (1991)

Background and aim

Definition

Dopamine

A neurotransmitter involved in movement, motivation and processing information; unusual levels of activity are linked to several conditions.

  1. People with schizophrenia show under-activity of the prefrontal cortex, the part of the brain used for planning, reasoning and switching strategy.
  2. On the dopamine hypothesis, dopamine activity is what drives that prefrontal work, so weak prefrontal activity should go with weak dopamine signalling there.
  3. If that is right, a drug that stimulates dopamine ought to raise prefrontal activity and improve scores on a task the prefrontal cortex is needed for.
  4. Amphetamine is one such drug, because it increases the amount of dopamine acting at the synapse.
  5. Aim: to investigate activity in the prefrontal cortices of people with schizophrenia.
Key Idea
  • Giving amphetamine raised dopamine activity, and prefrontal activity went up while card sorting scores improved.
  • That rise happened even though overall blood flow in the brain fell, so the effect was specific to the prefrontal region under cognitive demand.
  • The study is used as support for the dopamine hypothesis, because it ties dopamine activity to how well the brain performs a thinking task.

Method

Definition

Placebo

A dummy treatment that contains no active drug, given so that a participant does not know whether they have had the real drug and the drug's effect can be compared fairly.

  1. Design: a laboratory experiment using repeated measures, so each participant was tested with and without amphetamine on two different days.
  2. Counterbalanced: half the participants took amphetamine on the first day and half took the placebo first, which cancels out order effects such as practice on the task.
  3. The placebo meant participants did not know which they had been given, so their own expectations could not shape their scores.
  4. Sample: ten in-patients from mental health research wards in the USA.
  5. Controls: every participant's symptoms had already been stabilised with medication before testing began.
  6. None of them was physically ill, and none was using alcohol or other drugs.
Note
  • Repeated measures means the same ten people produced both sets of scores, so the comparison is within a person rather than between two groups.
  • Every participant was already on medication, which is a control here and a limitation later, because that medication was also acting on dopamine.

Variables and apparatus

  1. Independent variable: whether participants were given a placebo or 0.25 mg/kg of oral dextroamphetamine.
  2. Dependent variable: performance on a cognitive task, the Wisconsin Card Sort Test, which needs the prefrontal cortex to plan and to switch strategy.
  3. In that test a person sorts cards by a rule they are never told, and the rule changes without warning, so they have to notice the change and switch.
  4. Apparatus: brain activity was measured by a SPECT (single-photon emission computed tomography) scan, which tracks regional cerebral blood flow as a sign of how hard an area is working.
  5. Participants also performed a sensori-motor control task alongside the cognitive task, so any change could be tied to the cognitive demand rather than to general arousal.
Example
  • Dopaminergic neurons release dopamine into the synapse, and amphetamine increases how much dopamine acts there.
  • More dopamine at the synapse means more signal reaching the next neuron in the prefrontal cortex.

Results

  1. There was a significant difference between the amphetamine and placebo conditions on the cognitive task, but not on the sensori-motor task.
  2. Amphetamine significantly increased prefrontal cortex activity during the cognitive task, and task scores were higher.
  3. That rise happened despite the drug reducing overall blood flow in the brain, so the effect was specific to the prefrontal region under cognitive demand.

Conclusions

  1. Dopamine modulates and enhances cortical activity, since amphetamine stimulates dopamine activity and prefrontal activity went up.
  2. The prefrontal under-activity seen in schizophrenia is therefore at least partly reversible by dopaminergic means.
  3. Link to the theory: this supports the dopamine hypothesis, the biological explanation of schizophrenia, in which dopamine activity at the synapse shapes how the brain functions.
Common Mistake
  • This is a laboratory experiment rather than a natural experiment, because the researchers decided who got the drug and who got the placebo.
  • Blood flow did not rise everywhere, because overall blood flow fell while prefrontal activity during the cognitive task rose.

Criticisms

  1. Strength, the design: repeated measures removes individual differences, counterbalancing cancels order effects, and the placebo blinds the participant.
  2. Strength, the data: scan readings and task scores are objective and quantitative, so another team could repeat the study and check the figures.
  3. Strength, the control task: the sensori-motor task pins the effect to the cognitive demand rather than to general arousal from the drug.
  4. Sample: ten in-patients is too small to represent everyone diagnosed with schizophrenia.
  5. Validity: sorting cards to a hidden rule is too artificial to say much about everyday thinking.
  6. Extraneous variable: the medication that stabilised symptoms was itself altering dopamine activity, so its effect cannot be separated from the amphetamine's.
  7. Dated findings: schizophrenia is diagnosed differently now, so these ten patients may not match who would be diagnosed today.
  8. Ethics: using scanning equipment for research alone carries risk, and so does giving amphetamine to people who are already unwell.
  9. Nature and nurture: the biological explanation sits on the nature side of this debate, because it explains schizophrenia through dopamine and brain function.
  10. That leaves out nurture, such as upbringing, stressful life events and rejection by other people.
Note
  • Amphetamine is used here as a research tool rather than as a treatment, since raising dopamine can also make positive symptoms worse.
  • One study cannot carry the dopamine hypothesis on its own, so it sits alongside the evidence from anti-psychotic drugs.

Turning this into marks

  1. When two criticisms are asked for, make them genuinely separate rather than one criticism rephrased.
  2. Name the SPECT scan and the Wisconsin Card Sort Test, because a general reference to a brain scanning study does not secure the knowledge mark.
  3. The mark most often lost is reporting the rise in prefrontal activity without saying that overall blood flow fell.
Self review
  • State the aim of Daniel et al. (1991).
  • Why is this a laboratory experiment rather than a natural experiment?
  • What happened to prefrontal activity, and what happened to overall blood flow?
  • Why was a sensori-motor control task included?
  • How does the study support the dopamine hypothesis?
PreviousNext

How was this guide?

Teach Genie

Review 3.2.6 Schizophrenia research study: Daniel et al. (1991) by teaching Genie

Teach it back in your own words, spot gaps, and remember it better.

Start teaching
Genie and Baby Genie

Lesson

Recap your knowledge with an interactive lesson

8 minute activity

Start lesson

Daniel et al. (1991) investigated activity in the prefrontal cortices of people with schizophrenia. The prefrontal cortex is involved in planning, reasoning and switching strategy, and reduced activity in this region is associated with cognitive and some negative symptoms of schizophrenia.

The dopamine hypothesis is pathway-specific rather than the claim that dopamine generally drives prefrontal functioning. Reduced dopamine activity in the mesocortical pathway, which projects to the prefrontal cortex, is associated with cognitive and negative symptoms. In contrast, increased dopamine activity in the mesolimbic pathway is associated with positive symptoms. Therefore, increasing dopamine is not predicted to improve every aspect of schizophrenia or necessarily to improve prefrontal performance.

Amphetamine was used as a research tool because it increases the amount of dopamine acting at synapses. Its effects could therefore test how increased dopamine activity relates to prefrontal activity and performance on a cognitive task, but the prediction was not that it would improve all symptoms or all aspects of prefrontal functioning.

Flashcards

Remember key concepts with flashcards

23 flashcards

Practice flashcards

What was the aim of Daniel et al. (1991)?

3.2.6 Schizophrenia research study: Daniel et al. (1991) Revision Guide

  1. GCSE
  2. /Psychology
  3. /3.2.6 Schizophrenia research study: Daniel et al. (1991)

Revision notes for OCR GCSE Psychology 3.2.6 Schizophrenia research study: Daniel et al. (1991): explanations and worked examples.

Revision guides