Describe and evaluate the dopamine hypothesis of schizophrenia

The dopamine hypothesis is an explanation for schizophrenia, which believes that the disease is caused by increased levels of the neurotransmitter. However, it has been revised and added to multiple times, as scientific advancements have been made. The first version stated that increased dopamine activity was the cause of schizophrenia and noted that the D2 receptor was the most significant in responding to it, however it failed to identify any specific brain areas that this would occur in and neglected the fact that differences in dopamine abnormalities could cause either positive or negative symptoms.

The simplistic nature of version one of the dopamine hypothesis led to Davis’ version two in 1991, which had newer and more credible evidence. This evidence identified that schizophrenia habitually presents itself after an increase in sub-cortical dopamine, especially in the striatum and specifically with the D2 receptor. This suggested that abnormalities in in the prefrontal cortex may have been causing the abnormalities in the limbic system and identified how abnormalities can cause different symptoms. Nonetheless, this version was still deemed to be over simplified and biologically reductionist.

Further advancements led to a third version of the dopamine hypothesis, which is our most accurate and scientifically credible explanation to date. It identified that most schizophrenics have abnormally high presynaptic dopamine production in their striatum due to also tending to have 10-20% higher levels, than usual, of D2 receptors there. Additionally, this idea of D2 receptor occupancy being linked to the development of psychosis was confirmed with the evidence having been collated from living schizophrenic human brains not just from the deceased or animals.

This links to a major criticism of this study as, whilst the evidence for version three may come from living brains, much of the evidence for version two has come from animal lesion or post mortem studies which means that it has been indirectly collated. Furthermore, we are not necessarily able to generalise their findings to humans as we cannot assume that dead or animal brains will react to damage in the same way as living human brains.

Leading on from this, the dopamine hypothesis is said to be biologically reductionist as it over simplifies the biology involved in the transmission of dopamine, and does not take individual differences such as patients’ genetics and hormones, and their respective effects, into consideration. Moreover, it assumes that all schizophrenics’ receptors work with the same degree of sensitivity, which is simply not a generalisation we can make.

It makes the assumption that dopamine causes schizophrenia based simply upon evidence that lower dopamine levels can reduce its symptoms. This is problematic as it poses an issue with cause and effect as just because dopamine causes certain symptoms, it doesn’t mean that the underlying cause of schizophrenia is anything to do with it. Further evidence is required to prove that dopamine is the cause of schizophrenia, and at the moments there is no direct way of measuring it, only indirect, so once more the evidence is based too heavily upon assumptions. To understand schizophrenia and its causes more thoroughly we must take into account the extensive role that our environment plays e.g. by analysing whether a patient has a history of abuse, victimisation or failure as each of these may change their brain chemistry as opposed to the disease itself, and so we must recognise that our behaviour and experiences may lead to abnormalities.