1. Evaluation of the dopamine hypothesis (biological explanation)
Using SODAR – using slides 16-23

2. Worksheet – learning space
Complete using the information provided on the learning space, the slides and your own research
Remember the importance of having enough A01

3. S O D A R

4. Dopamine hypothesis (SOAR)

5. Support for dopamine hypothesis
Post mortems of brains of people who had have had schizophrenia show a higher density of dopamine receptors is in certain parts of the brain (cerebral cortex) than those who have not suffered from schizophrenia (Owen et al. 1978)
Wong et al. (1980) – PET brain scans show increase of dopamine in patients of schizophrenia (research details for more A01)
Medication – symptoms are treated with dopamine antagonists (chlorpromazine)
Blocks dopamine receptors therefore less dopamine is taken up therefore the effects of excess dopamine is avoided
Helps alleviate positive symptoms in 60% of cases
SZ- more sensitive to the action of dopamine
Seeman (2013) People diagnosed with schizophrenia may have a higher number of D2 receptors with a high affinity to dopamine
More likely to bind to the neurotransmitter when it is present in the synapse
More likely to overreact to the presence of the neurotransmitter
This may result from a combination of increased presynaptic neural pruning, a high release of dopamine (Howes et al., 2012), altered numbers of dopamine D2 receptors (Seeman, 2013a), and/or an increased sensitivity of the D2 receptor to dopamine (Seeman, 2011).
This view is supported by the fact that the positive symptoms of delusions and hallucinations are alleviated in the majority of patients by D2-blocking medications.

6. Support: Leiberman et al. 1987
Those treated with dopamine enhancing levodopa for Parkinson's disease can experience psychotic side effects mimicking the symptoms of schizophrenia.
Up to 75% of patients with schizophrenia have increased signs and symptoms of their psychosis upon challenge with moderate doses of methylphenidate or amphetamine or other dopamine- like compounds, all given at doses at which control normal volunteers do not have any psychologically disturbing effects (Kammen, Docherty and Bunney 1982)
However not all users of amphetamine suffer from psychotic symptoms – Suggesting there is something different about how people’s brains react to dopamine

7. However 40% don’t have a response to dopamine antagonist medication – therefore the medication still lowers levels of dopamine but doesn’t always treat the disorder. Therefore there must be another cause of symptoms.
There is lack of impact on the negative symptoms
PET scans show that blocking dopamine receptors does not always remove symptoms
The scans show that the medication does not alleviate symptoms if the patient has had schizophrenia for 10 years or more even if the block is 90% effective
If the medication is administered early on in the disorder then more than 90% of patients respond

8. Amphetamines only produce symptoms that are like the positive symptoms and not the negative symptoms which suggests that dopamine hypothesis is not sufficient enough explanations
People experience symptoms of mania when taking amphetamines which is not a symptom experience by those with schizophrenia

9. This hypothesis does not negate the dopamine hypothesis
This hypothesis does not negate the dopamine hypothesis. Perhaps scientists should be looking at both neurotransmitters?
Difference theories
Other neurotransmitters may be involved in the development of schizophrenia linked to psychosis
The glutamate hypothesis
Those who take PCS ‘angel dust’ experience symptoms similar to those who have schizophrenia (positive symptoms and negative e.g. psychotic state and inability to pay attention and changes cognitive function)
PCP acts at one of the receptors that glutamate stimulates to block the affects of glutamine
From this it is hypothesis that schizophrenia symptoms may be due to a deficiency in this receptor (NDMA) and the receptor cannot properly be stimulated by glutamate (Moghaddam and Javitt 2012)
In the last 15 years 26 placebo controlled double blind trials have been carried out to identify if sarcosine can reduce symptoms of schizophrenia
Sarcosine helps increase NMDA receptor activation
Effects of this drug on negative symptoms are highly significant. Effects on cognition, positive symptoms, and general psychopathology are more modest but still significant (Lin, 2010)
Enhancing NMDAR function can significantly reduce symptoms in schizophrenia, especially those least responsive to existing antipsychotic medications.
Correlation only
Perhaps neurotransmitter functioning takes place because of other issues in our genetic make up or stimulation from the environment
Perhaps stressful events in life can trigger production of excess dopamine or the blocking of glutamate.

10. Application - usefulness
Why is the explanation useful to those with schizophrenia?
Dopamine antagonist medication is seen to work 60% of the time (Leiberman, 1987)
This ensures there distress is decreased and that their wellbeing is enhanced.
Point: People with Schizophrenia are more sensitive to dopamine uptake (Carlsson)
How can this be used as evidence for usefulness?

11. Does this theory oversimplify the explanation of schizophrenia?
Reductionism
This is a reductionist explanation as it explains the disorder by the smallest possible ‘unit’ of explanations – an imbalance of a single neurotransmitter.
This ignores the complex interrelationship between neurotransmitter levels and other biological, psychological and social factors that may influence the whether an individual may develop the disorder.
Evidence on the next slide…..

12. Seeman (2014) a more holistic/interactionist explanation should be used
“It is further here suggested that dopaminergic overdrive is a necessary step on the path between initial causation and symptom expression. As such, therapeutic interventions need to focus on preventing dopamine overstimulation through a combination of means:
biological (dampening dopamine release and transmission)
psychological (muting stress that is mediated through dopamine pathways)
sociological (alleviating poverty and discrimination, which raise dopamine activity in large swaths of the population).”

13. ‘To what extent does the dopamine hypothesis explain Schizophrenia

14. Further evaluation Psychology as science?
Use of psychological knowledge in society? Change towards a medical treatment as it has a physical cause has led to the development of antipsychotic medication. Enhance well being and decrease distress. Prevents hospitalisation.
Ethics of research with patients with schizophrenia - informed consent?

15. Link to developmental psychology
5.1.6 of specification requires this link
The neurochemical balance can be affected by many things during development
Genes from conception
Prenatal factors – maternal illness or exposure to infection o lack of nutrition (Opler & Susser, 2005)
Chemical exposure (i.e. drugs)
Schizophrenia developed in late adolescence and early adulthood – why is it important for developmental psychologists to take this into account?

16. Individual differences
5.1.5 of the specification
Symptoms are diverse
Individual differences are not taken into account in this explanation
Not everyone will have the same reaction on treatment
Leiberman et al. (1987)
‘However 40% don’t have a response to dopamine antagonist medication – therefore the medication still lowers levels of dopamine but doesn’t always treat the disorder. Therefore there must be another cause of symptoms.’