Schizophrenia - Biological Explanations: Dopamine Hypothesis Flashcards
Describe the initial dopamine hypothesis
- proposed individuals with schizophrenia had too much dopamine
- symptoms were related to high levels of dopamine
- but drugs that lowered dopamine levels had little to no effect on those who suffered mainly from negative symptoms
What did scientists discover that led to the revised dopamine hypothesis
- due to drugs having little to no effect on individuals with negative sympotoms we developed this hypothesis
- scientists found that there were several subtypes of dopamine receptor sites (D1 to 5)
- widely distributed in the cerebral cortex and in the limbic system
- this then led to the ‘revised dopamine hypothesis’
Describe the 2 revised dopamine hypothesis
1) Hyperdopaminergia = overstimulation of Mesolimbic pathway
2) hypodeopaminergia = dysfunction in mesocortical pathway
Describe the revised dopamine hypothesis - Mesolimbic pathway
- carries signals from VTA (ventral tegmental area) to the nucleus accumbens
- too much dopamine, resulting from neurones that fire too quickly/much, causing overstimulation
- which causes positive symptoms such as hallucinations and dellusions
Describe the revised dopamine hypothesis - Mesocortical pathway
- carries signals from VTA (ventral tegmental area) to the frontal lobe
- it is a vital pathway in emotional responses, motivation and cognition
- too little dopamine in D1 receptors of the frontal lobe causes cognitive impairments and negative symptoms of schizophrenia
Explain what the researchers did, found and why it supports the dopamine hypothesis in Grilly’s research
- in 1950s
- Parkinson Disease patients were given the drug L-dopa
- they found the patient showed schizophrenic-type symptoms
- it supports the hypothesis because if non-schizophrenic patients are given a drug that increases dopamine and they show symptoms of schizophrenia, it suggests that excessive dopamine is the cause of schizophrenia
Explain what the researchers did, found and why it supports the dopamine hypothesis in Griffith et al’s research
- 1968
- induced psychosis in non-schizophrenic volunteers by administering dextro-amphetamine (increases dopamine)
- found onset of paranoid delusions and cold/detached emotions
- supports the hypothesis because if the dopamine hypothesis wasn’t true then normal people would behave normally when administered a drug to increase dopamine.
- but the change in behaviour suggests too much dopamine causes schizophrenia
Explain what the researchers did, found and why it supports the dopamine hypothesis in Seeman and Lee’s research
- 1975
- researched the effect of antipsychotic drugs on D2 receptors. Reduces schizophrenic symptoms as the drug is a blocking agent (antagonist)
- patients show less symptoms
- this supports the hypothesis because dopamine is received at D2 receptor sites on the post-synaptic neurone (ending) which allows the message to produce more dopamine. If this is blocked then positive symptoms reduce, suggesting D2 receptors are involved in schizophrenia
Explain what the researchers did, found and why it supports the dopamine hypothesis in Davis et al’s research
- 1991
- tested schizophrenics and found too little dopamine in D1 receptors in frontal lobe showed cognitive impairments and negative symptoms
- this supports the hypothesis because if D1 receptors have too little dopamine the people experience negative symptoms of schizophrenia. Suggesting that the mesocortical pathway is linked to schizophrenia
What is the alternative evidence that shows a weakness of the dopamine hypothesis by using genetics
- Gottesman et al. (1991) family study
- dopamine isn’t the only explanation — what causes this imbalance in the first place?
- As genetically similarity increases so did the probability of both individuals having schizophrenia
- he found a concordance rate of 48% between identical (monozygotic) twins and 17% for non-identical (dizygotic) twins
- and later research in 2014 found there are 108 genetic locis associated with schizophrenia
Can dopamine be measured
- Not directly, however…
- since dopamine is metabolised into HVA (Homovallinic acid)
- it can be measured in cerebral fluid via a lumbar puncture
Why is measuring HVA problematic
- diet and drugs affect metabolite levels meaning individual differences may vary levels of HVA
- questions the validity of dopamine hypothesis
What is the alternative evidence that shows a weakness of the dopamine hypothesis by using other neurotransmitters
- Carlson (2000)
- is dopamine the sole neurotransmitter?
- he found low receptors of glutamate may cause high levels of serotonin which then causes high levels of dopamine
- therefore, in the Mesolimbic pathway, low glutamate = low GABA = high dopamine (positive symptoms)
- in the mesocortical pathway, low glutamate = low dopamine (negative symptoms)
What is the alternative evidence that shows a weakness of the dopamine hypothesis by using PET scans
- Copolov and Crook (2000)
- Pet scans showed no difference in dopamine activity of those with or without schizophrenia
- suggesting that the dopamine hypothesis is not an exclusive theory
Is the dopamine hypothesis Valid or not valid? Evaluate
Invalid
P: The dopamine hypothesis can be seen as invalid because it doesn’t explain what causes the imbalance of dopamine in the first place, which causes schizophrenia
E: Gottesman et al. (1991) suggests it may be genetic, finding a concordance rate of 48% in Monozygotic twins and 17% in Dizygotic twins. As well as this, research in 2014 has since found 108 genetic loci associated with schizophrenia
T: Therefore because the hypothesis cannot explain this, the dopamine hypothesis would seem to be invalid and incomplete and therefore a weak explanation of schizophrenia
COUNTER: It has provided a good baseline of knowledge that scientists used to develop anti-psychotics in order to combat the positive symptoms of schizophrenia, which has seen to be effective in most cases, showing a sense of validity behind what the hypothesis suggests causes schizophrenia.
