Discuss biological explanations into schizophrenia.

(8+16)

AO1 Dopamine hypothesis

Dopamine is one the many different neurotransmitters that operate in the brain. The dopamine hypothesis states that messages from neurons that transmit dopamine, fire too easily or too often, leading to the characteristic symptoms of schizophrenia. For example over activity in the basal ganglia

and frontal cortex (areas concerned with initiating and control of movement) may cause the unusual and unpredictable behaviours seem in schizophrenics. Schizophrenics are thought have abnormally high number of D2 receptors on receiving neurons, resulting in more dopamine binding and therefore more neurons firing. Dopamine neurons play a key role in guiding attention, so disturbances in this process may well lead to the problems relating to attention, perception and thought found in people with schizophrenia (Comer).

AO2

There is some research support for the dopamine hypothesis, that can come from various sources one in particular being from amphetamines, as they increase dopamine function and produces schizophrenia-like symptoms e.g. hallucinations. Laruelle et al. administered amphetamine to individuals with schizophrenia and those without and the patients with schizophrenia showed a greater increase in dopamine transmission than those without schizophrenia.

AO2 

Further support for the dopamine hypothesis comes from Winterer and Weinberger who found schizophrenics often have an abnormal dopamine ratio of D1:D2 receptors, which causes disruption in the processing of internal and external stimuli and this links to some of the symptoms of schizophrenia.

AO2 

There is a lack of consistency in the evidence for example brain-imaging studies have produced rather variable results. Farde et al. (1990) found no difference in the number of dopamine receptors between schizophrenia and a control group. This lack of reliability may be due to the reductionist approach of the theory as it only focuses on the role of dopamine and not taking into account other factors such as the role that other neurotransmitters may have such as serotonin.

For example one of the most effective drugs in treating schizophrenia is clozapine. This drug has its major effect on the serotonin system rather than the dopamine system, suggesting other neurotransmitters could also be causal factors in sz.

AO1 GENES 

Another explanation for schizophrenia is genetics, one way of testing this theory is through twin studies. If monozygotic twins, who share 100% of their genes are more concordant than dizygotic twins who share only 50% of their genes then this suggests that genetics may have an involvement in schizophrenia. Gottesman conducted a meta-analysis of 40 studies that included considerable differences in the severity of the symptoms of schizophrenia. The concordance rate was 48% when a monozygotic twin had schizophrenia, but only 17% when a dyzygotic twin had schizophrenia. Gottesman also reported that the concordance rate for MZ twins reared apart was similar to those reared together. These findings strongly suggest that genetic factors are important – the reason why MZ’s have a much higher concordance rate than DZ’s is because they are much more similar genetically.

AO2

A criticism of the twin studies is that, it assumes that the environments of MZ twins and DZ twins are equivalent. Therefore it is assumed that the greater concordance rate for SZ between MZ twins is a product of greater genetic similarity rather than greater environmental similarity. However as Joseph points out, it is widely accepted that MZ twins are treated more similarly, encounter more similar environments and experience more ‘identity confusion’ than DZ twins. As a result there is reason to believe that the differences in concordance rates between MZ and DZ twins reflect nothing more than the environmental differences that distinguish the two types of twins.