One biological explanation which has been proposed for SZ is the Dopamine Hypothesis. This hypothesis suggests that SZ results from over-activity in the head dopamine (DA) systems. The excess in the brains DA systems is both an excess of DA existence released from neurons into the synapse, and an excess of DA receptors, meaning that the excess DA released is draped into the nervous system. Schizophrenic patients also tend to have emergence DA sensitivity, meaning that even if their brains DA systems were working at a normal level their symptoms world power still be present.
The Dopamine Hypothesis has a large-scale amount of support. Wong et al (1986) carried out a interpret use PET scans on live participants. They appoint a two-fold increase in the tightfistedness of DA receptor sites in SZ patients who had neer been treated by drugs, compared to patients who had been treated with drugs, and a control group. However, whilst this study supports the Dopamine Hypothesis, as it suggests that an excess of DA causes SZ, no some other researchers have been able to replicate the results that Wong got, seriously calling into call into question the reliability of the results.
Another piece of supporting evidence comes from run et al (1992), who found that Clozapine- one of the most clinically impelling treatments for SZ- has been shown by PET scans to occupy DA receptor sites, suggesting that DA is one of the main causes of SZ. However, Clozapine is not 100% effective, suggesting that DA is not the lonesome(prenominal) cause of SZ. Also, Clozapine treats both the arbitrary and negative symptoms of SZ, with only the positive symptoms seeming to be think to excess DA levels, again suggesting DA is not the only cause of SZ.
Seaman (1987) reviewed a number of studies involving post-mortems of SZ patients. He found that overall, SZ patients have an increase in DA receptor density of between...If you want to get a full essay, order it on our website: Ordercustompaper.com
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