Evaluation of the dopamine hypothesis for schizophrenia
- Goldman Rakic et al (2004): Found a link between low levels of dopamine in the prefrontal cortex and
negative symptoms
- Leucht et al (2015): Reviewed 212 studies in a meta-analysis on the effectiveness of antipsychotics that
normalise dopamine levels. Found that the treatment of symptoms with drugs were much more
effective than a placebo.
- Iverson: Examined the brains of deceased schizophrenic patients. Found that they all had a higher
concentration of dopamine, especially in the limbic system, compared with brains of people without
S schizophrenia
- PET scans: PET scans have shown lower levels of dopamine in PFC of schizophrenics
- Neurotransmitters: Glutamate is found in lower levels in people with schizophrenia. Its presence
reduces dopamine levels (However it can also create confounding variables. It could be lower levels of
glutamate causes schizophrenia and that the increase in dopamine levels is incidental).
- Drugs: Amphetamines and L-Dopa can increase levels of dopamine in the brain. They are known to
cause schizophrenic-like symptoms. LSD and other illicit drugs produce the same effect.
Drug treatments: Has allowed drug treatments to be developed in order to reduce dopamine, and
therefore improve symptoms of schizophrenia.
P
I
Supports biological approach: Shows that the levels of neurotransmitters in our brain can cause
symptoms of schizophrenia, showing that our physiological state can influence our psychological state.
Contradicts behaviourist approach: Shows that not all behaviour is learned from the environment as
imbalances in our neurotransmitters can make us act in certain ways
Contradicts cognitive approach: Shows that behaviour doesn’t just occur from information processing.
A Behaviour can occur due to imbalances in our neurotransmitters.
C Owen et al: Conducted an autopsy on a patient with schizophrenia and found there were more
dopamine receptors. Therefore, there may be just be more dopamine receptors as opposed to more
dopamine
Farde et al (1990): Found no difference between the dopamine levels of people with schizophrenia
compared to ‘healthy’ people
Noll (2009): Found that one third of patients don’t respond to drugs that block dopamine. Means that
other neurotransmitters may be involved. Lowers external validity and generalisability of theory as it
shows that it doesn’t apply to everyone .
Ripke et al: Found that some genes that effect other neurotransmitters are also linked to schizophrenia.
This means that there are confounding variables so we cannot draw a clear correlation between
- Goldman Rakic et al (2004): Found a link between low levels of dopamine in the prefrontal cortex and
negative symptoms
- Leucht et al (2015): Reviewed 212 studies in a meta-analysis on the effectiveness of antipsychotics that
normalise dopamine levels. Found that the treatment of symptoms with drugs were much more
effective than a placebo.
- Iverson: Examined the brains of deceased schizophrenic patients. Found that they all had a higher
concentration of dopamine, especially in the limbic system, compared with brains of people without
S schizophrenia
- PET scans: PET scans have shown lower levels of dopamine in PFC of schizophrenics
- Neurotransmitters: Glutamate is found in lower levels in people with schizophrenia. Its presence
reduces dopamine levels (However it can also create confounding variables. It could be lower levels of
glutamate causes schizophrenia and that the increase in dopamine levels is incidental).
- Drugs: Amphetamines and L-Dopa can increase levels of dopamine in the brain. They are known to
cause schizophrenic-like symptoms. LSD and other illicit drugs produce the same effect.
Drug treatments: Has allowed drug treatments to be developed in order to reduce dopamine, and
therefore improve symptoms of schizophrenia.
P
I
Supports biological approach: Shows that the levels of neurotransmitters in our brain can cause
symptoms of schizophrenia, showing that our physiological state can influence our psychological state.
Contradicts behaviourist approach: Shows that not all behaviour is learned from the environment as
imbalances in our neurotransmitters can make us act in certain ways
Contradicts cognitive approach: Shows that behaviour doesn’t just occur from information processing.
A Behaviour can occur due to imbalances in our neurotransmitters.
C Owen et al: Conducted an autopsy on a patient with schizophrenia and found there were more
dopamine receptors. Therefore, there may be just be more dopamine receptors as opposed to more
dopamine
Farde et al (1990): Found no difference between the dopamine levels of people with schizophrenia
compared to ‘healthy’ people
Noll (2009): Found that one third of patients don’t respond to drugs that block dopamine. Means that
other neurotransmitters may be involved. Lowers external validity and generalisability of theory as it
shows that it doesn’t apply to everyone .
Ripke et al: Found that some genes that effect other neurotransmitters are also linked to schizophrenia.
This means that there are confounding variables so we cannot draw a clear correlation between
