Biological explanations: Neural Correlates: The Dopamine Hypothesis

Dopamine

• Is a neurotransmitter that helps control the brain’s rewards and pleasure centres

• It is excitatory in that it increases brain activity

• Stimulant drugs such as caffeine, cocaine and amphetamines increase dopamine activity in the brain, increasing feelings of alertness

• Regulates movement and emotional responses. Enables us to not only see rewards but to take action to move towards them (motivation)

Dopamine Hypothesis

• Suggests that SZ is caused by imbalances in dopamine. Different symptoms are thought to be related to either too much or too little dopamine activity in specific brain areas

• Abnormally high dopamine activity (hyperdopaminergia) in the subcortex. Symptoms of speech poverty and auditory hallucinations can be explained by an excess of dopamine receptors in Broca’s area

• Abnormally low dopamine activity (hypodopaminergia) in the prefrontal cortex. (This is the brain area that is responsible for thinking and decision making). This is associated with the negative symptoms of avolition and lack of motivation

• While these seem to contradict each other, it may be that BOTH hyperdopaminergia and hypodopaminergia are correct explanations for SZ. General imbalances of dopamine are involved in SZ with high or low levels in different areas of the brain causing the positive and negative symptoms

Research evidence for dopamine hypothesis: Hyperdopaminergia

Timmons and Hamilton (1990) report that high doses of amphetamine ( drug that stimulates dopamine activity) can result in an acute psychosis resembling SZ in clinically normal people. This amphetamine psychosis can be treated with chlorpromazine

• This shows that increasing dopamine activity through amphetamine use leads to SZ like symptoms which can be treated by reducing dopamine activity

Research evidence for the dopamine hypothesis: Hypodopaminergia

Meador-Woodruff et al (1997) carried out post-mortem investigation of 16 patients who had suffered from SZ and compared them to 9 controls. They found dramatic decreases in dopamine receptors in the prefrontal cortex

• This shows that dopamine receptors in SZ patients would have resulted in reduced dopamine activity, suggesting that this was the cause of their SZ

However there is evidence to suggest that dopamine does not provide a complete explanation for SZ

Some of the genes identified in Ripke’s genome study code for the production of other neurotransmitters, so although dopamine plays an important role so do other neurotransmitters. Current research is focused in investigating the role of a neurotransmitter called glutamate

Application to treatment and implications to the economy

• If SZ is caused by imbalances of dopamine in the brain, drug treatment that acts as dopamine activity should effectively treat symptoms of SZ. Research suggests that antipsychotic drugs are effective in treating the positive symptoms of SZ

• This has a positive impact for the economy because drug therapy is a lot cheaper for the NHS than talking such as CBT patients can take medicine on their own without a therapist needing to be present

Neural correlates: Enlarged ventricles

• Neural correlates are patterns of structure or activity in the brain that occur alongside an experience

• Ventricles are cavities that produce and store cerebrospinal fluid which provides the brain with nutrients and removes waste

• Individuals with SZ typically have abnormally large ventricles in their brains. As a result the brains of those with SZ are lighter than usual due to a reduction in grey matter

• On average the ventricles in a person with SZ are approximately 15% larger than normal.

Supporting evidence

Suddath et al (1990) compared MRI scans of MZ twins where one twin had developed SZ. The images showed that the schizophrenic twin consistently had enlarged ventricles and reduced volume in the anterior hypothalamus than the non schizophrenic twin. These differences were so pronounced they were easily identifiable in 12/15 pairs of twins.

There is a correlation-causation problem with neural correlates

• Research has suggested that changes to ventricle volume occurs AFTER the onset of schizophrenia and that individuals who are high risk for the development of SZ do not have enlarged ventricles

• This suggests that changes to the ventricles are due to neurodegeneration as a result of developing SZ, not a cause of the disorder