Psychology: Clinical – Content (AJW)
Evaluate the function of neurotransmitters in explaining schizophrenia This essay is just over 600 words and would probably be a bout the right length for a 12 marker, (15 mins of writing time).Chain of reason that contains AO1 knowledge and understanding of the hypothesis (103)One strength of the original dopamine hypothesis, which suggested that an excess of dopamine may be responsible for the symptoms of schizophrenia, is that it is supported by studies such as that of Wise and Stein who found that schizophrenics who died in accidents had abnormally low levels of beta-hydroxlase, an enzyme which breaks down dopamine after its release. This is an important finding because it suggests that people with schizophrenia may have enhanced levels of dopamine molecules in the synaptic gap following activation of the post synaptic cell as there is not enough enzyme to break down left over molecules post transmission. Introducing competing arguments (56)One the one hand, whilst this finding does seem to support the original dopamine hypothesis, many scientists would view this finding as weak support as the hypothesis as the findings are correlational in nature; it is not clear whether schizophrenia is caused by low levels of beta-hydroxlase or whether this is an effect the condition itself. Another chain of reason with embedded AO1 (57)This said, further support comes from Timmons and Hamilton in their study on the effects of amphetamines, which are dopamine agonists and therefore enhance dopamine activity. In non-schizophrenic controls, the drug brings about schizophrenic-like symptoms. If artificially raising dopamine levels brings about schizophrenic symptoms in normal people then may be dopamine levels are naturally high in schizophrenics. Using applications to real life (in addition to research evidence) (166)Another strength of original hypothesis is that it has helped in terms of understanding how schizophrenia can be treated and this is important as it means that people with this conditions may be able to live freely in their communities rather than in an institution for example. For example, Barlow and Durand have shown that 60% of people experience relief through neuroleptic drugs such as chlorpromazine which binds to dopamine receptor sites, without activating them and thus block dopamine uptake. However, this evidence can also be used to reveal problems with the original version of the hypothesis as there are 40% of people whose dopamine levels are being decreased but this has no impact of their condition, similarly many others only experience relief from positive but not form negative symptoms, suggesting it is wrong to only focus on only one neurotransmitter. This is further supported by the fact that clozapine which also blocks serotonin receptors is successful for treatment resistant schizophrenics and also reduces negative parison to other theories (165); another way of introducing competing argumentsThe more recent version of the dopamine hypothesis by Davis (1991) has been particularly helpful in understanding the link between hypodopaminergia in the frontal lobes and the meso-cortical pathways and hyperdopaminergic in the striatum and meso-limbic pathways and also in focusing on the role of serotonin in regulating dopamine. However, it is important to note that theories which focus solely on the role of neurotransmitters go little way in explaining why people from specific groups in society, such as second generation immigrants for example, are more likely to be diagnosed with schizophrenia. This suggests that environmental factors such as social stress may impact our biology making some people more prone to psychosis. Perhaps the most useful update to the dopamine hypothesis has come from Howes and Kapur who highlight the importance of socio-cultural and cognitive factors, in determining how a person makes sense of aberrant salience caused by dopaminergic abnormality and thus accounting for the cultural diversity in the many and varied manifestations of schizophrenia.Balanced conclusion (91)In conclusion, it can be seen that the dopamine hypothesis has come a long way since its conception in the 1960s by Rossum and much of the research which demonstrated problems with the original hypothesis have been accounted for in the newer versions, which have been helpful in explaining a wide range of positive and negative symptoms and have considered the ways in which neurotransmitters interact. As the glutamate hypothesis now takes hold, it is likely that the future may bring yet more breakthroughs and hopefully treatments for this devastating condition. ................
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