Dopamine hypothesis

Dopamine AO1

• Neurotransmitter responsible for mood regulation, reward & motivation

• High levels of dopamine receptors at the synapse are associated with sz

• Low levels are associated with Parkinsons disease

Increase

• Increase in dopamine at the mesolimbic pathway contributes to positive symptoms

Decrease

Decrease in dopamine at the mesocortical pathway contributes to negative symptoms

Strengths AO3

• P - drug studies support

• E - amphetamines are dopamine agonists, meaning they increase the production of dopamine in the brain, whilst Levodopa increases dopamine synthesis and is used to treat Parkinson’s disease. Research has shown that high doses of amphetamines can induce hallucinations and delusions in non-patients and significantly worsen positive symptoms in individuals with schizophrenia. Similarly, patients treated with L-DOPA have been observed to develop psychotic symptoms resembling schizophrenia. T

• T - this provides strong empirical support for the dopamine hypothesis, as artificially increasing dopamine levels leads to schizophrenia-like symptoms, demonstrating a direct link between dopamine activity and psychosis and increasing the validity of the explanatio

• P - post-mortem research support

• E - researchers such as Pearlson et al found via PET scans that people diagnosed with schizophrenia had significantly higher numbers of dopamine D2 receptors in key brain areas compared to non-schizophrenic controls. This suggests that increased dopamine receptor density may lead to heightened dopamine activity, which could explain the presence of positive symptoms such as hallucinations and delusions.

• T - because post-mortem studies allow researchers to directly examine brain chemistry and receptor levels, this evidence is highly detailed and objective, supporting the dopamine hypothesis & strengthening its biological validity

Limitations AO3

• P - arguably reductionist

• E - dopamine hypothesis takes a complex phenomenon, such as sz, & reduces it down to an overly simplified explanation which focuses solely on internal causes, such as abnormal dopamine functioning, ignoring all possible external causes. This oversimplifies the disorder, which is known to be multifactorial. For example, research has shown that factors such as cognition, genes and dysfunctional family communication are associated with an increased risk of developing schizophrenia.

• T - By focusing narrowly on dopamine levels, the dopamine hypothesis fails to account for how social and cognitive factors contribute to symptom onset and relapse, limiting its explanatory power and reducing its usefulness as a complete explanation of schizophrenia. Perhaps a more sophisticated response is the interactionist approach which uses the diathesis stress model, which acknowledges both internal & external causes (a biological vulnerability & environmental stressor), providing a more nuanced & holistic explanation of sz than the dopamine hypothesis. These approaches are more effective in guiding treatment, as they support the use of combined therapies (e.g. antipsychotic medication alongside CBT).

• P - issues of causality

• E - studies show that people with schizophrenia often have higher levels of dopamine synthesis and increased D2 receptor density, but it is unclear whether this dopamine dysfunction is the cause of schizophrenia or a consequence of the disorder (or its treatment). It is possible that living with schizophrenia, or experiencing symptoms such as stress and psychosis, may itself alter dopamine functioning. In addition, much of the supporting evidence comes from the effects of antipsychotic drugs, which reduce dopamine activity and alleviate positive symptoms. However, this only shows that dopamine is involved in symptom expression, not that dopamine imbalance is the original cause. Similarly, drugs such as amphetamine, which increase dopamine levels, can induce psychotic-like symptoms, but this again demonstrates correlation rather than causation.

• T - as a cause & effect relationship cannot be established, the dopamine hypothesis may overstate dopamine’s causal role, reducing its explanatory validity.