Dopamine Hypothesis

Q: The Revised Dopamine Hypothesis & Evaluation

**Davis and Kahn (1991)** proposed that the positive symptoms of schizophrenia are caused by an excess of dopamine in subcortical areas of the brain, particularly in the mesolimbic pathway.

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The Dopamine Hypothesis

The dopamine hypothesis suggests that an excess of the neurotransmitter dopamine in certain regions of the brain is associated with the positive symptoms of schizophrenia.

What is the dopamine hypothesis?

Messages from neurons that transmit dopamine fire too easily or too often, leading to hallucinations and delusions that are the characteristic positive symptoms of schizophrenia.
Schizophrenics are thought to have abnormally high numbers of D2 receptors on receiving neurons, resulting in more dopamine binding and therefore more neurons firing. The key role played by dopamine was highlighted in two sources of evidence.

Drugs that increase dopaminergic activity

Amphetamine is a dopamine agonist i.e. it stimulates nerve cells containing dopamine, causing the synapse to be flooded with this neurotransmitter.
‘Normal’ individuals who are exposed to large doses of dopamine-releasing drugs such as amphetamines can develop the characteristic hallucinations and delusions of a schizophrenic episode.
This generally disappears with abstinence from the drug.

Grilly, 2002

Likewise, some people who suffer from Parkinson’s disease, a neurodegenerative disease categorised by low levels of dopamine, who take the drug L-Dopa to raise their dopamine levels have been found to develop schizophrenia type symptoms (Grilly, 2002).

Drugs that decrease dopaminergic activity

Although there are many different types of antipsychotic drug, they all have one thing in common, i.e. they block the activity of dopamine in the brain.
By reducing the activity in neural pathways of the brain that use dopamine as the neurotransmitter, these drugs eliminate symptoms such as hallucinations and delusions. The fact that these drugs (known as dopamine antagonists because they block its action) alleviated many of the symptoms of schizophrenia strengthened the case for the important role of dopamine in this disorder.

The Revised Dopamine Hypothesis & Evaluation

Davis and Kahn (1991) proposed that the positive symptoms of schizophrenia are caused by an excess of dopamine in subcortical areas of the brain, particularly in the mesolimbic pathway.

Revised dopamine hypothesis

The negative and cognitive symptoms of schizophrenia are thought to arise from a deficit of dopamine in areas of the prefrontal cortex (the mesocortical pathway). Evidence for this revised hypothesis comes from various sources.

Evidence: neural imaging

E.g. Patel et al (2010) used PET scans to assess dopamine levels in schizophrenic and normal individuals and found lower levels of dopamine in the dorsolateral prefrontal cortex of schizophrenic patients compared to their normal controls.

Evidence: animal studies

Wang and Deutch (2008) induced dopamine depletion in the prefrontal cortex in rats.
This resulted in cognitive impairment (e.g. memory deficits) that the researchers were able to reverse using olanzapine, an atypical antipsychotic drug thought to have beneficial effects on negative symptoms in humans.

Evaluation of the dopamine hypothesis

Strengths
- Antipsychotic drugs affect dopamine levels and successfully treat the symptoms of schizophrenia.
Limitations _ Moncrieff (2009) claims that evidence for the dopamine hypothesis of schizophrenia is far from conclusive.
- Noll (2009) claims there is strong evidence against both the original dopamine hypothesis and the revised dopamine hypothesis. He argues that antipsychotic drugs do not alleviate hallucinations and delusions in about one-third of people experiencing these problems.