Up Learn – A Level Psychology (AQA) – SCHIZOPHRENIA

Limitations of the Dopamine Hypothesis of Schizophrenia – Part 2

Moncrieff conducted a review of the evidence, and claimed that the evidence supporting the dopamine hypothesis is inconclusive for two reasons: First, she pointed out that drugs like amphetamines, which cause positive symptoms, affect other neurotransmitters as well as dopamine. So, we can’t be sure that it’s the increased dopamine that is causing these symptoms. Second, she pointed out that not all post-mortem studies report significant differences in levels of dopamine in the mesolimbic system of schizophrenic patients.

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Up Learn – A Level PsychologY (AQA)

Schizophrenia

1. Biological Explanations of Schizophrenia – Introduction (free trial)
2. Genetic Explanations of Schizophrenia (free trial)
3. The Genetic Explanation of Schizophrenia: Twin Studies (free trial)
4. The Genetic Explanation of Schizophrenia: Limitations of Twin Studies (free trial)
5. The Genetic Explanation of Schizophrenia: Adoption Studies (free trial)
6. The Genetic Explanation of Schizophrenia: Limitations of Adoption Studies (free trial)
7. Brain Abnormalities and Schizophrenia (free trial)
8. The Neural Correlates Hypothesis (free trial)
9. Neural Correlates: Study Support (free trial)
10. Effects of Medication on Brain Structure (free trial)
11. Individual Differences in Brain Abnormalities (free trial)
12. The Dopamine Hypothesis (free trial)
13. The Revised Dopamine Hypothesis (free trial)
14. The Dopamine Hypothesis: Study Support (free trial)
15. Limitations of the Dopamine Hypothesis – Part 1 (free trial)
16. Limitations of the Dopamine Hypothesis – Part 2
17. Biological Treatments for Schizophrenia: Antipsychotic Drugs (free trial)
18. How Antipsychotic Drugs Work (free trial)
19. Limitations of Traditional Antipsychotics: Side Effects (free trial)
20. Limitations of Traditional Antipsychotics: Negative Symptoms (free trial)
21. Typical and Atypical Antipsychotics (free trial)
22. Support for Atypical Antipsychotics (free trial)
23. Comparing Effects of Atypical Antipsychotics and Typical Antipsychotics (free trial)
24. Limitations of Atypical Antipsychotics: Effectiveness (free trial)

Last time, we looked at a limitation of the dopamine hypothesis…

One limitation of the dopamine hypothesis is that drugs that decrease dopamine don’t treat the symptoms of all patients with schizophrenia.

Noll reviewed drug studies in which patients with schizophrenia were given drugs that reduce dopamine activity.

They found that, for one third of patients, drugs that decrease the level of dopamine didn’t prevent hallucinations and delusions.

This suggests that high levels of dopamine in the mesolimbic system aren’t the only cause of positive symptoms.

Now, a second limitation of the dopamine hypothesis is that the evidence supporting the hypothesis isn’t always conclusive.

For example, in 2009, a researcher called Moncrieff reviewed the studies investigating the dopamine hypothesis.

Based on these studies, Moncrieff made two main criticisms of the dopamine hypothesis.

First, she pointed out that drugs that cause hallucinations and delusions, like… 

Drugs that cause hallucinations and delusions, like amphetamine, don’t just increase dopamine activity.

These drugs also affect the activity of other neurotransmitters, like serotonin, and noradrenaline.

So, it’s possible that hallucinations and delusions aren’t caused by increased dopamine activity…

But instead are caused by increased serotonin or noradrenaline!

Now, a second criticism made by Moncrieff is that there is little direct evidence that people with schizophrenia have an imbalance of dopamine activity…

Moncrieff reviewed the studies that had used post-mortem examinations to look at changes in dopamine levels in the brains of patients with schizophrenia. 

Now, we know that a post-mortem examination is…

A post-mortem examination is when a person’s brain is examined in detail after death, to look for evidence of brain abnormalities.

Now, according to the dopamine hypothesis, these studies should have found…

According to the dopamine hypothesis, these studies should have found increased levels of dopamine in the mesolimbic pathway, in the brains of patients with schizophrenia.

But, what Moncrieff actually found was that, although some post-mortem studies reported increased levels of dopamine in the mesolimbic pathway…

Lots of other studies reported no difference in the levels of dopamine in the mesolimbic pathway of patients with schizophrenia, compared to the control brains!

To sum up…

To sum up, we’ve now seen a second limitation of the dopamine hypothesis:

Moncrieff conducted a review of the evidence, and claimed that the evidence supporting the dopamine hypothesis is inconclusive for two reasons:

First, she pointed out that drugs like amphetamines, which cause positive symptoms, affect other neurotransmitters as well as dopamine. So, we can’t be sure that it’s the increased dopamine that is causing these symptoms.

Second, she pointed out that not all post-mortem studies report significant differences in levels of dopamine in the mesolimbic system of schizophrenic patients.