Neural correlates and the dopamine hypothesis | AQA A-Level Psychology Revision
- Revision Notes
- Aug 6
- 24 min read
Updated: 8 hours ago
For 7182 specification, first teach in September 2025
AQA A-Level Psychology | Free Revision Notes
Estimated study time: 60 minutes
These Neural correlates and the dopamine hypothesis A-Level Psychology revision notes explore how brain structure, brain activity and neurotransmitters may contribute to schizophrenia. You will examine the original and revised dopamine hypotheses, including excessive subcortical activity and reduced dopamine activity in cortical areas. You will also consider structural and functional brain correlates, evidence from medication and brain scanning, and the crucial problem that an association does not necessarily demonstrate causation. AQA requires both neural correlates and the dopamine hypothesis as biological explanations of schizophrenia.
Learning Objectives 🎯
By the end of this revision page, you should be able to:
Explain what psychologists mean by a neural correlate.
Distinguish structural, functional and neurochemical correlates.
Explain the original and revised dopamine hypotheses.
Link different patterns of dopamine activity to positive and negative symptoms.
Apply neural explanations to unfamiliar scenarios.
Evaluate neural explanations using research evidence, methodological issues and alternative explanations.
Revision Notes 📚
What are neural explanations?
A neural explanation proposes that schizophrenia is associated with differences in the brain.
These differences may involve:
Brain structure.
Activity in particular brain regions.
Communication between brain regions.
Neurotransmitter activity.
The number or sensitivity of receptor sites.
The dopamine hypothesis is therefore one neural explanation, but it is not the only one.
AQA’s specification identifies genetics and neural correlates, including the dopamine hypothesis, as the required biological explanations of schizophrenia.
The basic neural argument
A simplified neural explanation is:
altered brain structure or functioning → disrupted psychological processes → symptoms of schizophrenia
For example:
excessive dopamine activity in subcortical areas → unusual importance attached to experiences → hallucinations or delusions
However, this pathway is a theoretical explanation. Researchers must still determine whether the neural difference:
Caused the symptom.
Developed alongside the symptom.
Resulted from the condition.
Resulted from medication or another variable.
What is a neural correlate?
A neural correlate is a measurable feature of brain structure or functioning that is associated with a behaviour, experience or psychological condition.
The term can be separated into two parts:
Neural means relating to the brain or nervous system.
Correlate means something that varies alongside another variable.
For example, researchers might find that reduced activity in a particular brain region is associated with severe avolition.
This would be a neural correlate of avolition.
It would not automatically prove that reduced activity caused the avolition.
Correlation is not causation
This distinction is one of the most important ideas in the lesson.
A finding such as:
people experiencing severe negative symptoms show reduced activity in a particular brain region
could have several explanations:
Reduced brain activity caused the symptoms.
Experiencing the symptoms altered brain activity.
Medication affected both symptoms and brain activity.
Another factor caused both variables.
The observed association occurred only within a particular subgroup.
The careful conclusion is:
The neural difference is associated with the symptom.
The overconfident conclusion is:
The neural difference definitely causes the symptom.
Types of neural correlate
Type of neural correlate | What is measured? | Possible schizophrenia example |
Structural | Physical anatomy of the brain | Enlarged ventricles or reduced grey matter |
Functional | Activity within a brain region | Reduced activity in the prefrontal cortex |
Neurochemical | Activity of chemical messengers | Increased or reduced dopamine activity |
Receptor-based | Number, sensitivity or occupation of receptor sites | Altered activity at dopamine D2 receptors |
Structural neural correlates
Brain structure
A structural neural correlate is an anatomical characteristic associated with schizophrenia or one of its symptoms.
Researchers may compare:
The size of brain regions.
The volume of grey matter.
The size of fluid-filled spaces.
The thickness of parts of the cortex.
Structural connections between regions.
Past AQA mark schemes have recognised enlarged ventricles, reduced grey matter and reduced temporal or frontal lobe volume as relevant neural correlates of schizophrenia.
Enlarged ventricles
The brain contains fluid-filled spaces called ventricles.
Some people diagnosed with schizophrenia have been found to possess enlarged ventricles.
Larger ventricles may be associated with:
Reduced volume of surrounding brain tissue.
Changes in brain development.
Loss or reduction of grey matter.
Less efficient communication between brain areas.
This does not mean that enlarged ventricles are present in every person diagnosed with schizophrenia.
It also does not mean that enlarged ventricles are unique to schizophrenia.
Reduced grey matter
Grey matter contains many neuronal cell bodies and is involved in processing information.
Some brain-imaging research has identified reduced grey-matter volume among people diagnosed with schizophrenia.
Possible consequences may include disruption to:
Thinking.
Memory.
Decision-making.
Language.
Emotional processing.
Control of attention.
However, reduced grey matter is a broad finding. It does not show that one precise brain change produces every symptom.
Reduced frontal-lobe volume
The frontal lobes contribute to processes such as:
Planning.
Decision-making.
Inhibition.
Working memory.
Goal-directed behaviour.
Monitoring thoughts and actions.
Reduced volume or functioning in frontal areas may therefore be associated with:
Cognitive difficulties.
Reduced organisation.
Avolition.
Problems initiating behaviour.
Some forms of disordered speech.
This association should be expressed cautiously. Frontal-lobe differences are not a complete explanation of schizophrenia.
Reduced temporal-lobe volume
Temporal regions contribute to:
Auditory processing.
Language.
Memory.
Interpretation of sensory information.
Altered temporal functioning may therefore be associated with experiences such as auditory hallucinations.
This does not mean that damage to one temporal region automatically produces hallucinations.
Functional neural correlates
Brain activity
A functional neural correlate is an association between schizophrenia and the level or pattern of activity in a brain region.
Functional activity may be investigated using techniques such as:
Functional magnetic resonance imaging, or fMRI.
Positron emission tomography, or PET.
Electroencephalography, or EEG.
AQA mark schemes have recognised reduced activity in regions including the superior temporal gyrus, anterior cingulate gyrus and ventral striatum as relevant neural correlates.
The prefrontal cortex
The prefrontal cortex is involved in:
Planning.
Cognitive control.
Attention.
Decision-making.
Working memory.
Regulating behaviour.
Reduced dopamine activity or reduced functioning in this area may contribute to:
Difficulties organising thought.
Reduced goal-directed behaviour.
Speech poverty.
Avolition.
Cognitive impairment.
Reduced activity in the prefrontal cortex is sometimes described as hypofrontality.
The ventral striatum
The ventral striatum contributes to:
Motivation.
Reward anticipation.
Learning from rewarding outcomes.
Initiating goal-directed behaviour.
Reduced activity in the ventral striatum has been associated with negative symptoms, particularly avolition.
A possible pathway is:
reduced ventral-striatum activity → weaker anticipation of reward → reduced motivation to begin or continue activities
This might help explain why a person understands that an activity could be worthwhile but still struggles to initiate it.
The superior temporal gyrus
The superior temporal gyrus contributes to:
Processing sounds.
Language.
Interpreting speech.
Distinguishing internally and externally generated information.
Altered activity in this region may be associated with auditory hallucinations.
For example, internally generated speech might be experienced as if it came from an external source.
This overlaps with problems recognising internally generated thoughts.
The anterior cingulate gyrus
The anterior cingulate gyrus contributes to:
Directing attention.
Detecting conflict.
Monitoring errors.
Regulating emotion.
Selecting appropriate responses.
Abnormal activity in this region may be associated with difficulties:
Controlling attention.
Monitoring thoughts.
Distinguishing important from unimportant information.
Regulating emotional responses.
One symptom can involve several regions
A symptom such as a hallucination is unlikely to be produced by one isolated brain area.
It may involve interaction among systems responsible for:
Speech production.
Auditory processing.
Attention.
Memory.
Monitoring internal thoughts.
Assigning importance to experiences.
This makes network-based explanations more realistic than the claim that one “hallucination centre” causes the experience.
Neurotransmitters and synaptic transmission
What is a neurotransmitter?
A neurotransmitter is a chemical messenger that carries information between neurons.
Communication occurs at a synapse, the small gap between neurons.
The basic process is:
An electrical impulse reaches the presynaptic terminal.
Neurotransmitter is released into the synaptic cleft.
The neurotransmitter crosses the gap.
It binds to receptor sites on the postsynaptic neuron.
The postsynaptic neuron is affected.
Remaining neurotransmitter may be broken down or reabsorbed.
What is dopamine?
Dopamine is a neurotransmitter involved in several functions, including:
Motivation.
Reward.
Learning.
Movement.
Attention.
Assigning importance to experiences.
Dopamine does not have one single effect throughout the brain.
Its effects depend on:
The brain region.
The neural pathway.
The receptor type.
The amount released.
Receptor sensitivity.
Interactions with other neurotransmitters.
The dopamine hypothesis
The central claim
The dopamine hypothesis proposes that abnormal dopamine activity contributes to schizophrenia.
The earliest version focused mainly on excessive dopamine activity.
The modern account is more complex.
It proposes that schizophrenia may involve:
Excessive dopamine activity in some subcortical areas.
Reduced dopamine activity in cortical areas, particularly the prefrontal cortex.
Different patterns of activity associated with different symptoms.
Past AQA mark schemes explicitly recognise excessive subcortical dopamine alongside reduced cortical or prefrontal dopamine activity.
The original dopamine hypothesis
Excessive dopamine activity
The original hypothesis proposed that schizophrenia resulted from excessive dopamine activity throughout the brain.
Possible mechanisms included:
Too much dopamine being released.
Dopamine remaining active for too long.
An unusually large number of receptor sites.
Dopamine receptors being unusually sensitive.
This account was particularly useful for explaining positive symptoms.
Positive symptoms
Positive symptoms involve experiences or behaviours added to ordinary functioning, including:
Hallucinations.
Delusions.
The original hypothesis proposed:
excess dopamine activity → excessive neural stimulation → positive symptoms
However, the idea of too much dopamine everywhere is now regarded as oversimplified.
The revised dopamine hypothesis
Different activity in different pathways
The revised hypothesis recognises that dopamine activity may be:
Excessive in one pathway.
Reduced in another pathway.
Associated with different symptoms in different brain regions.
The central contrast is:
Pattern of dopamine activity | Main area | Symptoms most commonly linked |
Hyperdopaminergia | Subcortical regions | Positive symptoms |
Hypodopaminergia | Cortical regions, particularly the prefrontal cortex | Negative and cognitive symptoms |
Hyperdopaminergia
Hyperdopaminergia means unusually high dopamine activity.
Excessive dopamine activity in subcortical areas is associated with positive symptoms.
AQA mark schemes have referred specifically to increased activity in the subcortex and ventral tegmental area.
How excessive dopamine may contribute to positive symptoms
Excessive dopamine activity may cause ordinary experiences to gain excessive salience.
Salience means importance or significance.
For example:
A stranger looking across a room may seem intensely meaningful.
An unrelated television report may appear personally directed.
An internal thought may feel unusually vivid or externally produced.
A coincidence may seem like evidence of a conspiracy.
This could contribute to:
Delusions of reference.
Paranoid interpretations.
Auditory hallucinations.
Unusual beliefs.
A possible sequence is:
increased subcortical dopamine activity → excessive salience → unusual interpretation → positive symptom
Hypodopaminergia
Hypodopaminergia means unusually low dopamine activity.
Reduced dopamine activity in cortical areas, particularly the prefrontal cortex, is associated with negative and cognitive symptoms.
AQA mark schemes have also recognised low dopamine activity in the ventral striatum.
How reduced dopamine may contribute to negative symptoms
Low dopamine activity may reduce:
Motivation.
Reward anticipation.
Goal-directed behaviour.
Planning.
Cognitive flexibility.
Initiation of speech or action.
This could contribute to:
Avolition.
Speech poverty.
Reduced emotional engagement.
Social withdrawal.
Cognitive difficulties.
A possible sequence is:
reduced prefrontal or ventral-striatal dopamine activity → reduced motivation and cognitive control → negative symptoms
Dopamine pathways and symptoms
The key exam distinction is not simply “high dopamine” versus “low dopamine”.
It is:
different dopamine activity in different brain regions
Neural process | Possible psychological consequence | Possible symptom |
Excessive subcortical dopamine activity | Neutral events gain unusual significance | Delusions |
Excessive activation of auditory or salience networks | Internal information feels externally generated | Hallucinations |
Reduced prefrontal dopamine activity | Impaired planning and cognitive control | Disorganised behaviour or speech |
Reduced ventral-striatal activity | Weak reward anticipation | Avolition |
Reduced activity in language-related regions | Difficulty generating fluent language | Speech poverty |
The links are probabilistic, not guaranteed.
D2 receptors
What is a D2 receptor?
A D2 receptor is one type of receptor to which dopamine can bind.
D2 receptors are especially important in explanations and treatments of schizophrenia.
Typical antipsychotic medication reduces dopamine activity by blocking D2 receptor sites.
This prevents some dopamine molecules from activating the postsynaptic neuron.
AQA’s June 2024 assessment identified blocking dopamine receptor sites as the action of typical antipsychotics.
Receptor blockade
A simplified sequence is:
antipsychotic occupies D2 receptor → dopamine cannot bind as easily → postsynaptic stimulation is reduced → positive symptoms may decrease
The action of these drugs is explored fully in dopamine-blocking medication.
Receptor activity is not the same as dopamine quantity
High dopamine activity could result from:
Greater dopamine release.
More receptor sites.
Greater receptor sensitivity.
Reduced breakdown.
Reduced reuptake.
Altered communication within a pathway.
A student should therefore avoid assuming that the dopamine hypothesis refers only to the total amount of dopamine present.
Dopamine and positive symptoms
Hallucinations
Excessive subcortical dopamine activity may increase the significance attached to internally generated information.
A person may then interpret:
Inner speech.
Memories.
Intrusive thoughts.
Background sounds.
as externally produced or personally meaningful.
This can contribute to hallucinations.
Delusions
An ordinary event may attract excessive attention because of abnormal salience.
The person may then attempt to explain why the event feels so important.
For example:
A newsreader briefly looks towards the camera. The event feels highly significant, so the person concludes that the newsreader is sending them a message.
The delusion provides an interpretation of the unusually salient experience.
Further detail about these experiences is covered in hallucinations and delusions.
Dopamine and negative symptoms
Avolition
Avolition is a reduction in the ability to begin or continue goal-directed activity.
Reduced activity in reward and motivation systems may mean that:
Future rewards feel less motivating.
Activities require unusually high effort.
Goals fail to trigger action.
Behaviour is difficult to initiate.
This is not simply laziness.
Speech poverty
Reduced prefrontal functioning may affect:
Planning what to say.
Organising language.
Maintaining a line of thought.
Generating a detailed response.
This may contribute to reduced quantity or quality of speech.
Cognitive difficulties
Reduced cortical dopamine may also be associated with problems involving:
Attention.
Working memory.
Planning.
Decision-making.
Executive control.
These cognitive difficulties can worsen functional impairment even where positive symptoms are controlled.
Other neurotransmitters
Dopamine is not the whole story
Past AQA mark schemes have recognised the possible involvement of neurotransmitters including:
Glutamate.
Serotonin.
Acetylcholine.
This suggests that schizophrenia cannot be reduced to dopamine alone.
Glutamate
Glutamate is the brain’s main excitatory neurotransmitter.
Reduced glutamate activity, including reduced activity at NMDA receptors, has been associated with schizophrenia.
This may affect:
Learning.
Memory.
Brain development.
Communication between cortical regions.
Glutamate systems may also interact with dopamine systems.
Serotonin
Serotonin contributes to mood, perception and other psychological processes.
Some atypical antipsychotics act on both dopamine and serotonin receptors.
This suggests that altered serotonin activity may also be relevant.
The wider receptor actions of these drugs are explored in serotonin and broader receptor
A more complete neurochemical account
The modern position is therefore better represented as:
interacting abnormalities across several neurotransmitter systems contribute to vulnerability and symptoms
rather than:
schizophrenia is caused only by too much dopamine
Connecting genetic and neural explanations
Genes may influence:
Dopamine production.
Dopamine receptor development.
Brain structure.
Neural connectivity.
Sensitivity to stress.
Glutamate or serotonin functioning.
A possible biological pathway is:
inherited risk variants → altered neural development → abnormal neurotransmitter activity → increased vulnerability to symptoms
This connects neural explanations with inherited biological vulnerability.
However, genes do not determine a single fixed neural outcome.
Environmental experiences can also influence neural development and neurotransmitter functioning.
Applying neural explanations
Worked application: hallucinations
Marcus regularly hears a voice commenting on his behaviour. A scan suggests unusually high activity in a subcortical dopamine pathway.
A neural explanation would suggest:
Marcus shows a positive symptom.
Excessive subcortical dopamine activity is consistent with the revised dopamine hypothesis.
Increased dopamine may cause internally generated experiences to gain excessive salience.
Marcus may therefore interpret an internal experience as an external voice.
The scan does not prove that dopamine caused the hallucination.
Worked application: avolition
Leila spends most of the day inactive and struggles to begin even activities she previously enjoyed. Researchers find reduced activity in her ventral striatum.
A neural explanation would suggest:
Leila is showing avolition, a negative symptom.
The ventral striatum contributes to motivation and reward anticipation.
Reduced activity may mean that expected rewards fail to motivate behaviour.
This could contribute to her difficulty initiating activities.
Do not describe Leila as merely choosing not to act.
Worked application: medication
After taking an antipsychotic that blocks D2 receptors, Arun experiences fewer paranoid delusions.
This is consistent with the dopamine hypothesis because:
Paranoid delusions are positive symptoms.
The medication reduces dopamine action at D2 receptors.
Reduced symptoms suggest that excessive dopamine activity may have contributed.
However, successful treatment does not prove that dopamine originally caused the condition.
Worked application: mixed symptoms
Nadiya experiences persecutory delusions but also shows speech poverty and avolition.
The revised dopamine hypothesis can explain the mixture by proposing:
Excessive subcortical dopamine activity contributes to delusions.
Reduced cortical dopamine activity contributes to speech poverty and avolition.
Different neural pathways may be functioning differently at the same time.
Evaluating neural explanations
Strength: evidence from antipsychotic medication
Typical antipsychotics block dopamine receptors and can reduce positive symptoms.
This supports the dopamine hypothesis because:
The drug reduces dopamine activity.
Positive symptoms often decrease.
Excessive dopamine activity is therefore likely to be involved in at least some symptoms.
AQA mark schemes recognise the pharmacological action of effective antipsychotic drugs as relevant evidence for biological explanations.
Limitation: treatment does not prove cause
The effectiveness of a treatment does not demonstrate the original cause of a condition.
For example, pain may improve after taking a painkiller, but the pain was not necessarily caused by a lack of painkiller.
Similarly:
dopamine blockade reduces symptoms
does not logically prove:
excessive dopamine originally caused schizophrenia
Medication may interrupt a symptom-producing process without correcting the original cause.
Strength: objective brain-imaging evidence
MRI, fMRI and PET scans produce numerical biological data.
Researchers can measure:
Brain volume.
Ventricular size.
Regional activity.
Blood flow.
Receptor occupation.
This offers greater objectivity than relying only on interviews or observations.
Standardised scanning procedures can also improve:
Replicability.
Reliability.
Scientific credibility.
Limitation: scanning evidence is usually correlational
Researchers cannot randomly assign healthy participants to develop schizophrenia.
They normally compare naturally occurring groups:
People diagnosed with schizophrenia.
People without the diagnosis.
This means that differences in brain scans may be influenced by:
Medication.
Duration of illness.
Substance use.
Nutrition.
Sleep.
Stress.
Physical health.
Social isolation.
Cause and effect cannot be established confidently.
Past AQA mark schemes explicitly recognise the possibility that altered neurochemistry or neuroanatomy may be an effect rather than a cause.
Strength: the revised hypothesis explains different symptom types
The original hypothesis mainly explained positive symptoms.
The revised account is stronger because it proposes:
Excessive subcortical dopamine for positive symptoms.
Reduced cortical dopamine for negative and cognitive symptoms.
This gives the explanation greater scope.
It can account for a person experiencing positive and negative symptoms at the same time.
Limitation: dopamine activity is more complicated than high or low
Dopamine functioning varies across:
Pathways.
Receptor types.
Stages of the condition.
Individuals.
Symptoms.
Medication histories.
Some people may show one neural pattern but not another.
The explanation therefore becomes difficult to test as one simple hypothesis.
Limitation: not every person responds to dopamine-blocking drugs
Some people show limited improvement after taking medication that blocks dopamine receptors.
Others may experience improvement in positive symptoms but continue to show:
Avolition.
Speech poverty.
Cognitive difficulties.
Social impairment.
This suggests that dopamine dysfunction cannot explain every case or every symptom.
Strength: evidence from several biological methods converges
Neural explanations are supported by evidence from:
Structural brain scanning.
Functional brain scanning.
Neurochemical imaging.
Drug treatment.
Genetic research.
Studies of receptor activity.
When several methods indicate altered neural functioning, confidence in a biological contribution increases.
This is converging evidence.
Limitation: other neurotransmitters are involved
The involvement of glutamate, serotonin and acetylcholine challenges a dopamine-only account.
A more complete explanation may need to consider:
Interactions among neurotransmitters.
Effects of genes on neural development.
Environmental stress.
Cognitive processing.
The dopamine hypothesis remains useful, but it may explain one part of a larger system.
Limitation: neural correlates may be consequences
Avolition could lead to:
Reduced activity.
Less environmental stimulation.
Social isolation.
Changes in reward processing.
Long-term hallucinations or stress might also alter brain functioning.
Researchers therefore cannot assume:
neural difference → symptom
The direction could be:
symptom or lifestyle change → neural difference
or both variables could influence each other.
Limitation: schizophrenia is heterogeneous
People diagnosed with schizophrenia do not all experience the same symptoms.
One person may mainly experience:
Hallucinations.
Another may mainly experience:
Avolition and speech poverty.
Another may experience:
Cognitive disorganisation.
Different symptom profiles may involve different neural systems.
Treating schizophrenia as one uniform condition could hide important subgroups.
This problem is increased by co-morbidity and symptom overlap.
Limitation: diagnosis affects the validity of brain research
Brain-imaging studies depend on researchers placing participants into diagnostic groups.
If diagnosis is affected by:
Symptom overlap.
Co-morbidity.
Cultural bias.
Gender bias.
then a “schizophrenia group” may contain people with substantially different difficulties.
Apparent neural inconsistencies could partly result from inconsistent classification.
Limitation: biological reductionism
Neural explanations can be biologically reductionist because they reduce a complex condition to:
Dopamine release.
Receptor activity.
Brain volume.
Activity in individual regions.
This allows objective measurement and scientific testing.
However, it may overlook:
Personal meaning.
Thought processes.
Family relationships.
Trauma.
Social disadvantage.
Cultural context.
Environmental stress.
This links with levels of explanation and biological reductionism.
Value of reductionism
Reductionism also has advantages.
By breaking schizophrenia into measurable components, researchers can:
Form precise hypotheses.
Operationalise variables.
Use controlled methods.
Develop medications.
Compare biological subgroups.
Test treatment mechanisms.
AQA has recognised dopamine action at the synapse as a low-level biological explanation that can be contrasted with social-psychological explanations such as family dysfunction.
Limitation: biological determinism
A strong neural account may imply that symptoms are controlled entirely by brain chemistry.
This is biological determinism.
It can encourage the view that:
Symptoms are unavoidable.
Psychological intervention is pointless.
The individual has no control.
Recovery is unlikely.
However, neural functioning is influenced by:
Experience.
Learning.
Medication.
Stress.
Relationships.
Psychological treatment.
The account should therefore be probabilistic rather than completely deterministic.
This connects with biological determinism and human agency.
Strength: useful treatment applications
The dopamine hypothesis contributed to the development and use of antipsychotic medication.
Possible benefits include:
Reducing severe positive symptoms.
Supporting community living.
Making psychological therapy more accessible.
Reducing distress.
Decreasing the need for intensive care.
This gives the explanation practical value.
Limitation: medication may only manage symptoms
Medication may reduce symptoms without addressing:
Environmental stressors.
Distressing beliefs.
Social isolation.
Family conflict.
Coping strategies.
The original source of vulnerability.
Biological treatment may therefore need to be combined with psychological support.
Comparison with cognitive explanations
Neural explanations focus on biological processes, while cognitive explanations focus on dysfunctional information processing.
Neural explanation | Cognitive explanation |
Focuses on brain regions and neurotransmitters | Focuses on thinking and information processing |
Explains hallucinations through altered neural activity | Explains them through failure to recognise internal thoughts |
Uses scans and biological measures | Uses cognitive tasks and symptom reports |
Leads towards medication | Leads towards cognitive behaviour therapy |
Biologically reductionist | Cognitively reductionist |
May describe an underlying mechanism | May explain how a symptom is interpreted |
The explanations may be compatible:
altered neural functioning → dysfunctional cognitive processing → symptom
Comparison with family dysfunction
Neural explanations operate at a biological level.
Family communication and emotional climate operate at a social-psychological level.
The neural account may reduce blame placed on relatives, whereas family explanations can be interpreted as blaming family behaviour.
However, both accounts can become deterministic if presented as complete causes.
An interactionist account
A more complete account may involve:
genetic vulnerability + altered neural functioning + environmental stress + cognitive interpretation
For example:
A person inherits genetic vulnerability.
This affects dopamine or glutamate systems.
Stress increases neural instability.
Unusual experiences gain excessive salience.
Dysfunctional interpretations develop.
Symptoms emerge.
This is developed in combined biological and psychological accounts.
Research methods in neural investigations
MRI
Magnetic resonance imaging, or MRI, produces detailed images of brain structure.
It can be used to investigate:
Ventricular size.
Grey-matter volume.
Frontal-lobe volume.
Temporal-lobe volume.
Strength
MRI produces objective and detailed structural data.
Limitation
It identifies anatomy, not the psychological meaning of the difference.
fMRI
Functional magnetic resonance imaging, or fMRI, measures changes associated with blood oxygenation while a participant rests or completes a task.
It can identify which regions are more or less active.
Strength
Researchers can investigate functioning while a participant completes a cognitive task.
Limitation
Blood-flow changes are an indirect measure of neural activity.
PET
Positron emission tomography, or PET, can be used to study:
Metabolic activity.
Neurotransmitter synthesis.
Receptor activity.
Drug occupation of receptor sites.
Strength
PET can provide information about neurochemical processes.
Limitation
The procedure is expensive and involves exposure to a radioactive tracer.
Quasi-experimental comparisons
A study comparing diagnosed and non-diagnosed groups is usually a quasi-experiment.
The independent variable, diagnostic group, already exists.
Researchers cannot randomly allocate participants to schizophrenia.
This reduces control over participant variables.
Operationalisation
Neural variables must be operationalised precisely.
Examples include:
Ventricular volume measured in cubic centimetres.
Mean blood-oxygen response in a named region.
Percentage of D2 receptors occupied.
Symptom severity measured using a standardised scale.
Precise operationalisation improves replicability.
Participant variables
Groups may differ in ways unrelated to schizophrenia.
Researchers should attempt to match or control for:
Age.
Sex.
Medication.
Substance use.
Duration of illness.
Physical health.
Educational background.
Longitudinal research
A longitudinal study could scan people before and after the development of symptoms.
This may help establish whether neural differences appeared before the diagnosis.
However:
Large samples would be needed.
Many participants would never develop schizophrenia.
Repeated scanning would be expensive.
Attrition could reduce validity.
How to apply neural explanations in an exam
Step 1: Identify the symptom
Decide whether the scenario describes:
A positive symptom.
A negative symptom.
A cognitive difficulty.
Step 2: Select the relevant neural process
Possible links include:
Hallucination or delusion → excessive subcortical dopamine.
Avolition → reduced ventral-striatal activity.
Speech poverty → reduced prefrontal functioning.
Auditory hallucination → altered temporal-region activity.
Step 3: Explain the connection
Do not merely name the brain region.
Write:
“Reduced activity in the ventral striatum may weaken reward anticipation, making it harder for the person to initiate goal-directed behaviour. This could contribute to avolition.”
Step 4: Use cautious language
Use:
“May contribute.”
“Is associated with.”
“Is consistent with.”
“Supports the possibility.”
Avoid:
“Proves.”
“Always causes.”
“Every person has.”
“Inevitably produces.”
Step 5: Evaluate the inference
Where appropriate, add:
“Because the evidence is correlational, the scan cannot establish whether the neural difference caused the symptom.”
Exam paragraph structure
A strong evidence paragraph might follow this pattern:
Point: Antipsychotic medication supports the dopamine hypothesis.Evidence: Typical antipsychotics block D2 receptor sites and often reduce positive symptoms.Explanation: This is consistent with the claim that excessive dopamine activity contributes to hallucinations and delusions.Counterpoint: Treatment effectiveness does not prove the original cause, and some patients show limited improvement.Conclusion: Dopamine is involved in at least some symptoms, but it is unlikely to provide a complete explanation.
Overall conclusion
Neural explanations identify measurable associations between schizophrenia and:
Brain structure.
Regional brain activity.
Dopamine functioning.
Other neurotransmitter systems.
The revised dopamine hypothesis is stronger than the original account because it recognises that dopamine may be excessive in subcortical regions but reduced in cortical regions.
Evidence from brain scanning and antipsychotic medication supports a biological contribution. However, neural differences are not found uniformly, other neurotransmitters are involved, and most evidence is correlational.
The most defensible conclusion is:
Neural abnormalities contribute to schizophrenia, but they operate within a broader interaction of genetic, cognitive, psychological and environmental factors.
Hints from the Examiner Reports 💡
Examiner hint: Do not describe the dopamine hypothesis as simply “too much dopamine”.
A developed answer should distinguish:
Excessive activity in subcortical regions.
Reduced activity in cortical areas, especially the prefrontal cortex.
Low activity in the ventral striatum.
These distinctions are recognised in AQA mark schemes.
Examiner hint: Include D2 receptors when explaining dopamine-based treatment.
It is more precise to state:
“Typical antipsychotics block D2 dopamine receptor sites.”
than:
“The drugs remove dopamine.”
Examiner hint: In an application question, use details from the scenario. The June 2023 mark scheme credited a reduction in symptoms following medication as evidence suggesting a neurotransmitter or biological factor.
Examiner hint: Keep the explanation named in the question. The June 2022 examiner report noted that some students used the dopamine hypothesis when the question required a cognitive explanation.
Examiner hint: Do not merely identify a correlate. Explain its relevance.
Weak:
“The ventral striatum is involved.”
Stronger:
“Reduced ventral-striatum activity may weaken reward anticipation, contributing to avolition.”
Examiner hint: Methodological criticism must be connected to the explanation. Saying that a scanning study used a small sample is not enough. Explain that an unrepresentative sample reduces confidence that the neural correlate applies across people with different symptom profiles.
Examiner hint: Successful extended answers are organised and relevant. The June 2023 examiner report found that top-band responses often used several explanations or evaluative points concisely, rather than including long sections of irrelevant material.
Examiner hint: Avoid vague claims such as “drugs work”. State:
What the drug does.
Which symptom changes.
How this supports the explanation.
Why it does not prove causation.
Examiner hint: Use the word correlate accurately. A neural correlate is an association, not automatically an explanation of cause.
Common Mistakes ⚠️
Mistake: Saying schizophrenia is caused by too much dopamine everywhere
Why this is incorrect:
The revised hypothesis proposes different patterns in different brain regions.
How to improve:
Contrast excessive subcortical activity with reduced cortical activity.
Mistake: Treating a neural correlate as a proven cause
Why this is incorrect:
Most scan evidence is correlational.
How to improve:
State that the feature is associated with the symptom and discuss alternative directions of causality.
Mistake: Saying dopamine is a hormone
Why this is incorrect:
In this explanation, dopamine is discussed as a neurotransmitter.
How to improve:
Describe its role in carrying chemical signals between neurons.
Mistake: Saying D2 receptors release dopamine
Why this is incorrect:
Dopamine is released by the presynaptic neuron and binds to receptors.
How to improve:
Explain that D2 receptors are binding sites on neurons.
Mistake: Saying antipsychotics destroy dopamine
Why this is incorrect:
Typical antipsychotics block receptor sites and reduce dopamine action.
How to improve:
Describe receptor blockade accurately.
Mistake: Linking high dopamine to negative symptoms only
Why this is incorrect:
Excessive subcortical dopamine is primarily associated with positive symptoms.
How to improve:
Link reduced cortical or ventral-striatal activity to negative symptoms.
Mistake: Linking low dopamine to hallucinations without qualification
Why this is incorrect:
Positive symptoms are generally associated with excessive subcortical dopamine activity.
How to improve:
Select the appropriate pathway and symptom.
Mistake: Saying every person with schizophrenia has enlarged ventricles
Why this is incorrect:
Neural correlates describe group-level associations and are not universal.
How to improve:
Use “some people” or “on average”.
Mistake: Treating neural correlates and genes as identical
Why this is incorrect:
Genes are inherited DNA variations, whereas neural correlates are brain-based associations.
How to improve:
Explain that genes may influence neural development, but the two explanations are distinct.
Mistake: Claiming successful medication proves the dopamine hypothesis
Why this is incorrect:
A treatment can reduce symptoms without identifying the original cause.
How to improve:
State that drug effectiveness supports dopamine involvement but does not prove causation.
Mistake: Ignoring other neurotransmitters
Why this weakens the answer:
Glutamate, serotonin and other systems may contribute.
How to improve:
Use their involvement to evaluate a dopamine-only explanation.
Mistake: Saying brain scans directly show thoughts or hallucinations
Why this is incorrect:
Scans measure biological signals such as blood flow or metabolism.
How to improve:
Explain that psychologists infer psychological processes from patterns of activity.
Mistake: Describing reduced dopamine as no dopamine
Why this is incorrect:
Hypodopaminergia means lower-than-typical activity, not complete absence.
How to improve:
Use comparative language such as “reduced” or “lower activity”.
Mistake: Giving an unconnected methodological criticism
Why this loses marks:
The examiner needs to see how the issue affects the explanation.
How to improve:
Link medication confounds to uncertainty over whether the neural difference existed before treatment.
Mistake: Treating the explanation as fully deterministic
Why this is too strong:
Neural abnormalities increase vulnerability and interact with other factors.
How to improve:
Use probabilistic language and refer to interactionist explanations.
Exam-Style Questions ✍️
Questions
1. What is meant by a neural correlate?[2 marks]
2. Outline one structural neural correlate of schizophrenia.[3 marks]
3. Explain the revised dopamine hypothesis of schizophrenia.[4 marks]
4. Explain the difference between hyperdopaminergia and hypodopaminergia in schizophrenia.[4 marks]
5. Priya experiences persecutory delusions and believes that unrelated television reports contain messages for her.
Explain Priya’s experience using the dopamine hypothesis.[4 marks]
6. Daniel rarely begins activities and no longer seems motivated by events he previously enjoyed. A brain scan shows reduced activity in his ventral striatum.
Explain how this finding could account for Daniel’s behaviour.[4 marks]
7. Explain one strength and one limitation of using antipsychotic medication as evidence for the dopamine hypothesis.[6 marks]
8. Researchers record the following mean level of prefrontal activity during a planning task:
Group | Mean activity in arbitrary units |
Control group | 50 |
Participants with severe negative symptoms | 35 |
a) Calculate the percentage reduction in activity for participants with severe negative symptoms compared with the control group. Show your working.[2 marks]
b) Explain one conclusion the researchers could draw from these results.[2 marks]
c) Explain one reason why the researchers cannot conclude that reduced prefrontal activity caused the negative symptoms.[2 marks]
9. Explain one methodological limitation of using brain scans to investigate neural correlates of schizophrenia.[4 marks]
10. Compare the dopamine hypothesis with genetic explanations of schizophrenia.[8 marks]
11. Discuss neural correlates, including the dopamine hypothesis, as explanations for schizophrenia.[16 marks]
Answers and Mark Scheme
Question 1
Award up to two marks:
A neural correlate is a measurable feature or pattern of brain structure, functioning or neurochemistry.
It is associated with a behaviour, experience, symptom or psychological condition.
A definition must convey association. Do not credit an answer claiming that a correlate is necessarily a cause.
Question 2
Award up to three marks for one developed correlate.
Possible answer:
Enlarged ventricles have been identified among some people diagnosed with schizophrenia.
Ventricles are fluid-filled spaces within the brain.
Enlargement may be associated with reduced surrounding brain tissue or grey matter.
Alternative creditworthy examples include:
Reduced grey-matter volume.
Reduced frontal-lobe volume.
Reduced temporal-lobe volume.
Question 3
Award up to four marks:
The revised dopamine hypothesis proposes that dopamine activity differs across brain regions.
Excessive dopamine activity in subcortical areas is associated with positive symptoms.
Reduced dopamine activity in cortical areas, especially the prefrontal cortex, is associated with negative or cognitive symptoms.
Low activity in the ventral striatum may contribute to reduced motivation or avolition.
The account therefore replaces the simple claim that dopamine is excessive everywhere.
Question 4
Award up to four marks:
Hyperdopaminergia means unusually high dopamine activity.
In schizophrenia, it is associated particularly with subcortical regions and positive symptoms.
Hypodopaminergia means unusually low dopamine activity.
It is associated particularly with cortical or prefrontal regions and negative or cognitive symptoms.
Both patterns can occur within different pathways of the same brain.
Question 5
Award up to four marks:
Priya’s delusions are positive symptoms.
The revised dopamine hypothesis links positive symptoms with excessive subcortical dopamine activity.
Excess dopamine may cause ordinary events to gain excessive salience.
Priya may therefore experience an unrelated television report as highly significant.
She interprets this unusual significance as evidence that the report contains a personal message.
Question 6
Award up to four marks:
Daniel is showing avolition, a negative symptom.
The ventral striatum contributes to motivation and anticipation of reward.
Reduced activity may mean that expected rewards provide less motivation.
Daniel may therefore struggle to initiate or maintain goal-directed activity.
The scan is consistent with a neural correlate but does not establish causation.
Question 7
Award up to three marks for a developed strength and three for a developed limitation.
Possible strength:
Typical antipsychotics block D2 receptor sites and often reduce positive symptoms. This is consistent with the proposal that excessive dopamine activity contributes to hallucinations and delusions.
Possible limitation:
Treatment effectiveness does not prove the original cause. A drug may interrupt a process involved in symptoms without correcting the factor that initially produced schizophrenia. Some patients also show limited improvement.
Question 8a
5050−35×100=5015×100=30%
Award:
One mark for appropriate working.
One mark for 30%.
Question 8b
Award up to two marks:
Participants with severe negative symptoms showed lower mean prefrontal activity than controls.
This is consistent with an association between reduced prefrontal functioning and negative symptoms.
The result supports hypodopaminergic or hypofrontality accounts, where appropriately explained.
Do not credit a claim that the figures prove causation.
Question 8c
Award up to two marks:
The investigation is correlational or uses naturally occurring groups.
Reduced activity may be a consequence rather than a cause of the symptoms.
Medication, illness duration or another participant variable could explain the difference.
Question 9
Award up to four marks for one developed methodological limitation.
Possible answer:
Participants diagnosed with schizophrenia may have taken antipsychotic medication.
Medication changes dopamine activity and may also alter brain functioning.
A difference between diagnosed and control participants could therefore be caused partly by treatment.
This reduces confidence that the neural correlate existed before the symptoms developed.
Alternative creditworthy limitations include:
Correlational evidence.
Diagnostic heterogeneity.
Small or unrepresentative clinical samples.
fMRI providing an indirect measure.
Movement during scanning.
Differences in substance use or illness duration.
Question 10
A strong comparison may include:
Both are biological explanations.
Genetic explanations focus on inherited DNA variation.
The dopamine hypothesis focuses on neurotransmitter activity.
Genes may affect dopamine systems, making the explanations compatible.
Both can be biologically reductionist.
Both may be biologically deterministic if treated as complete explanations.
Genetic evidence comes from family, twin, adoption and molecular studies.
Neural evidence comes from brain scans, receptor studies and medication.
Both rely heavily on naturally occurring correlations.
Neither establishes that biology acts alone.
Genetic explanations describe inherited vulnerability.
The dopamine hypothesis may identify a mechanism through which that vulnerability is expressed.
Both lead towards biological treatment and early identification.
Both are more complete when combined with environmental stress.
Higher marks require direct comparisons rather than two separate descriptions.
Question 11
A strong response should include:
Knowledge and understanding
Definition of a neural correlate.
Distinction between correlation and causation.
Structural correlates:
Enlarged ventricles.
Reduced grey matter.
Reduced frontal or temporal volume.
Functional correlates:
Reduced prefrontal activity.
Reduced ventral-striatal activity.
Altered superior temporal or anterior cingulate activity.
Dopamine as a neurotransmitter.
Synaptic transmission and receptor sites.
D2 receptors.
Original dopamine hypothesis.
Revised dopamine hypothesis.
Excessive subcortical dopamine activity.
Reduced cortical or prefrontal dopamine activity.
Links to positive symptoms.
Links to negative and cognitive symptoms.
Possible involvement of glutamate, serotonin and other neurotransmitters.
Evaluation
Antipsychotic effectiveness supports dopamine involvement.
Treatment effectiveness does not prove original causation.
Not all patients respond to dopamine-blocking drugs.
Drugs may be more effective for positive than negative symptoms.
Objective evidence from MRI, fMRI and PET.
Brain scanning is largely correlational.
Neural abnormalities may be effects rather than causes.
Medication, duration and lifestyle are possible confounding variables.
The revised hypothesis has greater explanatory range than the original.
Different neural patterns may explain different symptom types.
Other neurotransmitters challenge a dopamine-only explanation.
Converging evidence increases confidence in biological involvement.
Schizophrenia is heterogeneous.
Problems with diagnosis weaken group comparisons.
Biological reductionism allows precise scientific investigation but may lose psychological and social context.
Biological determinism may create fatalism.
Practical applications include medication and early intervention.
Neural explanations can reduce blame but may increase biological stigma.
Cognitive, family and environmental explanations remain relevant.
An interactionist explanation provides a more complete account.
Higher-level responses will use accurate regional distinctions, develop the implications of evidence and avoid claiming that neural correlations automatically establish causation.
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