The dopamine theory Sz

What is dopamine?

Dopamine is a neurotransmitter in the brain involved in attention, emotion, movement and higher-cognitive functions, reward 

What is the original dopamine hypothesis theory?

The original hypothesis stated that Sz is associated with generally increased levels of dopamine in the brain 

What are antagonists and agonists?

• Antagonist – a drug that inhibits the effects of a neurotransmitter 
  (Typical antipsychotics would be antagonists, blocking dopamine receptors) 

• Agonist – a drug that facilitates the effects of a neurotransmitter 

What receptor in particular is associated with schizophrenia?

• An excess of D2 (dopamine) receptors

What are the technical terms for an increase and a decrease in dopamine levels?
And which pathways are these in?

• increase = hyperdopaminergia in the mesolimbic pathway

• decrease = hypodopaminergia in the mesocortical pathway

(hypO - mesOcOrtical)

Supporting evidence

AO1

• The original Dopamine hypothesis suggests that Schizophrenia is associated with increased levels of dopamine and dopamine receptors (particularly D2) in synapses in certain areas of the brain 

AO3

• This theory is supported by evidence from brain scans of Sz patients and non-Sz participants, which shows that when those with Sz are given amphetamines, there is a greater release of dopamine than in non-Sz people who are given amphetamines. These brain scans provide good evidence for this theory as they are objective and empirical. 

Conflicting

AO1

• Revised versions of the Dopamine hypothesis explores how an increase in dopamine (hyperdopaminergia) in the mesolimbic pathway may contribute to positive symptoms 

AO3

• However, there is evidence which refutes the hypothesis. For example, Alpert and Friedhoff (1980) found that some patients show no improvement after taking dopamine antagonists. PET scans have also shown that blocking dopamine receptors doesn’t always remove the symptoms in patients who had had Schizophrenia for 10 years or more – showing that the neurotransmitter explanation of schizophrenia may not account for everyone 

Opposing

AO1

• Decrease in dopamine (hypodopaminergia) in the mesocortical pathway may contribute to negative symptoms, such as low motivation, which other theories struggle to account for. 

AO3

• Opposing theories includes the social causation theory, which suggests that schizophrenia develops as a result of stressors in society e.g. urban living, low socioeconomic status and racial discrimination. The mere existence of other strong theories undermines the credibility of this theory – for example, the diathesis-stress model suggests schizophrenia is a result of both biological vulnerability and environmental stressors.  

Usefulness

AO1

• Research in the 2000s started to focus on the role of other neurotransmitters including GABA, which regulates glutamate and serotonin 

AO3

• Useful in leading to the creation of drugs to reduce the impact of schizophrenic symptoms. 

  Typical antipsychotics (e.g. chlorpromazine) reduce dopamine transmission to reduce the impact of positive symptoms, whilst atypical antipsychotics alleviate negative symptoms by affecting serotonin and glutamate. 
  The importance of these drugs is that they provide effective treatment for patients, aiding their quality of life 

Testability

The use of neuroimaging and brain scans allows a scientific and objective approach to testing this theory 

Simplicity

AO1

• The dopamine hypothesis should not be seen as an explanation of Sz, but an explanation of 'psychosis proneness’ 

AO3

The dopamine hypothesis is a reductionist explanation of Sz because many other factors are at play - as even other neurotransmitters impact upon schizophrenia (shown by clopazine, which targets serotonin) 

Conclusion

The newest view is that dopamine dysregulation in the striatum is linked with psychosis, but that interactions between genes, environmental and sociocultural factors should be taken into account. 

Description of the function of neurotransmitters in relation to schizophrenia [3]

• the dopamine hypothesis states that those with too much dopamine in the mesolimbic pathway will have positive symptoms of schizophrenia

• A higher number of D2 receptors in the brains means that more dopamine will bind to the receptors leading to schizophrenia

• a decrease of glutamate in the mesolimbic pathway in people with schizophrenia no longer inhibits dopamine, leading to an excess of dopamine