Dopamine Hypothesis

The dopamine hypothesis origniated from observations of the dopamine-blocking actions of early neuroleptic drugs. The hypothesis states that the brains of schizophrenics produce more dopamine than non-schizophrenics. Furthermore, PET scans reveal the D2 receptor is overactive in a schizophrenics brain. 

Radioactively labelled L-dopa and adminstered to schizophrenics and a control group of individuals who had not been diagnosed with schizophrenia. The evidence shhowed that L-dopa was taken up far more quicker in participants with a diagnosis of schizophrenia. This supports the dopamine hypothesis's principle that schizophrenics have more dopamine activity in the brain. 

Autopsies have revealed that people with schizophrenia have a larger than usual number of dopamine receptors, indicating that perhaps it's the recepetor sites onsetting schizophrenia rather than the level of neurotransmitter therefore criticising the principles of the dopamine hypothesis. 

Further research supports this conclusion: Strange 1992 as the autopsies from this study revealed that schizophrenics did have increased dopamine receptors who had never taken any anti-psychotic medication. 

It could be argued that perhaps it is not the neurotransmitter that causes an individual to develop schizophrenia but it is schizophrenia that causes the changes in neurotransmitter functioning in the brain. 

Research into this area is unfalsifiable as we cannot see which order it came as it's too complex conseqently limiting the validity of the principles of the dopamine hypothesis. 

There is a lack of correspondence between taking the drug and signs of clinical effectiveness. It takes 4 weeks to see any signs of the drug working when anti-psychotic drugs begin to block dopamine receptors immedieatly. 

This difference cannot be explained and as a result it could be suggested that perhaps there are other biological mechanisms involved which trigger the onset of schizophrenia rather than just dopamine production alone. 

The dopamine hypothesis can be seen as reductionist because it takes a complex disorder such as schizophrenia and breaks the cause down into a single simple componenet such as the level of dopamine. 

1/3 of diagnosed schizophrenics do not respond to any drug treatment because of this the validity of the principles of the dopamine hypothesis can be questioned. Other factors such as cognition and stressful environmental factors could contribute to the onset of schizophrenia and therefore a more holisitic bio-socio-psycho approach needs to be considered when treating diagnosed schizophrenics. 

It is thought that schizophrenia might be inherited, research into genetics has presented a possible link between schizophrenia and genes, and therefore suggesting that the complex disorder may be passed on from one generation to the next via genes. 

They found significant differences in MZ and DZ twins in their concordance rates of schizophrenia and also found that MZ twins were more similiar in their diagnosis. 

This suggests that the closer the relationship between two individuals the greater the likelihood that if one of them is diagnosed with schizophrenia the other individual will develop the disorder to, due to their genetic similiarity, supporting the principle of genes causing the onset of schizophrenia. 

A criticism of this study is that concordance rates were not a 100%. The evidence of this research could support an alternative explanation such as diathesis stress model which states that genetic factors lower the threshold for stress coping and environmental triggers may be needed to start the development of this disorder.

However, this study gas internal validity because the researchers used multiple research methods to ensure their diagnosis was correct and so they were definetly measuring what they aimed to measure. If psychology is a science, it needs to have high internal validity. 

Researched adopted away offspring of biological mothers who had been diagnosed with schizophrenia compared to a control group. Results showed that 7% of children of those who had a biological mother diagnosed with schiziphrenia were also diagnosed with disorder compared to 1.5% of the control group.

If the principle of genetics was entirely valid concordance rates should be a 100% suggesting other factors contribute to the onset of schizophrenia. Wahlberg et al supports this as the evidence from this study was reviewed again and new evidence showed children at genetic risk for schizophrenia are less likely to show abnormality if their adoptive family provided a support environment. This indicates there may be a genetic-environmental interaction which causes individuals to develop schizophrenia. 

Found high rates of diagnosis for chronic schizophrenia in adoptees whose biological parents had the same diagnosis even though they were adopted by 'healthy' parents. 

This rules out environmental factors and questions the validity of the diathesis stress model as the adoptees adopted by 'healthy' parents. As a result, this presenets strong evidence for a genetic component in the onset of schizophrenia. 

Since the inception of brain imaging in the form of PET, MRI and CAT scans, evidence has suggested that individuals with schizophrenia have structural differences in the brain compared to individuals who don't have schizophrenia. 

Found decreased brain weight and enlarged ventricles, which are that cavaties in the brain which hold the cerebrospinal fluid.

Also found enlarged ventricles, along with hippocampal volumes. The hippocampus is the part of brain involved in learning and memory. 

Found abnormalities in the frontal and prefrontal cortex (part of the brain involved in problem solving and high-level reasoning), the basal ganglia (movement and emotions) and the hippocampus (learning and memory). 

The advanced technology used in these studies offers high objectivity which if psychology is a science, should be able to achieve. Furthermore, reliability is offered because of this objectivity as the technology would produce the same results if the experiment was done again. 

Research into the area of brain structure can be considered inconclusive as it is ambigious to whether an abnormal brainstructure causes schizophrenia or schizophrenia leads to an abnormal brain structure. As a consequence, this limitis the validity of evidence from research into brain structure. 

Used MRI scans to obtain pitcures of MZ twins who are schizophrenic and MZ twins who are not schizophrenic. He found MZ twins who were schizophrenic had enlarged ventricles and a reduced hypothalamus. The differences in in brain structure were so large 12/15 twins could easily be identified as schizophrenic. 

This evidence suggests there is wider academic credibility for enlarged ventricles determining the likelihood of schizophrenia developing.

Did a longitudinal correlational study and found that anti-psychotic drugs have a measurable affect in brain tissue loss over time. This could limit possible supporting studies of brain structure because it could be the effect of drugs that change the strucure of the brain therefore limiting the validity of research. 

If brain structure was the sole cause of schizophrenia, it fails to explain why 35% of diagnosed schizophrenics are classified as 'much improved'. Reduction in brain volume and other strucutres is permanent and according to the principle schizophrenics should not able to improve, this suggests that perhaps there are other causes involved in the onset of schizophrenia and a more holisitc approach needs to be considered when explaining schizophrenia.