Literature into account to explain why these changes occur.

Literature
agrees that the dopamine hypothesis has contributed to a significant understanding
of the underlying mechanisms of schizophrenia due dopaminergic dysregulation in
specific pre frontal brain regions (Brisch et al., 2014). Schizophrenia has been centered
around dopamine activity for several decades, psychosis at the forefront of
research. It is important to understand that schizophrenia is more than a state
of psychosis, as both negative and cognitive symptoms are leading causes of
individuals having a poor quality of life, and inability to function (Lin et al., 2013). The dopamine hypothesis III
enables an array of factors biological and environmental to be taken into
consideration in the development of schizophrenia. However, it must be noted
that even Howes and Kapur (2009) admit themselves that the dopamine hypothesis III
gravitates towards “psychosis – in – schizophrenia” (p.556), suggesting that it
is mainly concerned with positive symptoms. Recent vivo imaging studies has
allowed dopaminergic functioning to be assessed in the pre synaptic, leading
away from the idea that the disorder is not just due to elevations in D2
receptors (Kambeitz
et al., 2013). The biggest question is that, although
dopamine dysregulation has numerous implications into drugs treatments, it
fails to acknowledge what may be driving these these alterations. Therefore, this indicates
that other neurotransmitters such as glutamate dysfunction must be taken into
account to explain why these changes occur.   

 

To fully
comprehend the latest dopamine hypothesis, it must be acknowledged that it has
come a long way since it was first introduced as the dopamine receptor
hypothesis due to the discovery of antipsychotic drugs in dampening dopamine
levels. However, by focusing on blocking excess dopamine receptors to control psychosis,
it was far too simplistic to explain such a complex disorder as no other
possible factors were taken into consideration. Furthermore, Davis et al (1991)
incorporated regional specificity, and found that the effects of abnormalities
in dopamine function vary depending on brain region. Although the hypothesis lacked
framework, these findings helped to guide and develop the dopamine hypothesis
III.

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The dopamine
hypothesis III takes into account an array of factors that all contribute to
increasing an individual’s vulnerability level in developing schizophrenia. These
include ‘hits’ resulting in dopamine dysregulation, presynaptic dopamine
dysregulation, sociocultural factors, and psychosis through aberrant salience. Howes
and Kapur (2009) found an abnormally large amount of D2/D3 receptors in
individuals with schizophrenia (10%-20% increase) in comparison to a healthy control
group. This indicates that an increase in dopamine sensitivity may be due to
larger quantity of synaptic receptors thus in turn increasing dopamine
transmission due to increased receptors. Vivo imaging studies show that
blocking these receptors (especially D2) are vital in controlling psychotic symptoms
by the use of antipsychotics. Many schizophrenics have been found to be sensitive
to elevations in dopaminergic drugs such an amphetamine (Seeman, 2011). Amphetamine
has also been found to cause psychosis even in healthy individuals. Support comes
from animal models as studies indicate there are high-affinity states of D2
receptors giving implication into treating psychosis with antipsychotics that
target these specific regions (Seeman, 2006). Seeman (2006) found that administering
amphetamine led to hypersensitivity and elevated D2 receptors in the striatum. This
gives great support to increased levels of dopamine and the extent to which it
can explain schizophrenia. Medhus et al (2015) found that 33% of 12 patients
went onto develop schizophrenia after being administrated amphetamine. Although
a relatively low percentage, it gives insight into how dysregulation of
dopamine through drugs such as amphetamine can eventually cause healthy patients
to develop schizophrenic symptoms. Further supporting the idea that amphetamine
increases psychotic symptoms comes from schizophrenic patients.  Schizophrenics have also been acknowledged in
their sensitivity towards dopamine stimulants, with 74%-78% of individuals
having worse symptoms when administered to them (Seeman and Seeman, 2014). Research with controls and
patients indicates awareness into the risk of increased psychotic symptoms due
to elevated dopamine levels. Based on such evidence, it is clear to say that
elevated D2 receptors and heightened dopaminergic sensitivity is a cause of
psychotic symptoms seen in schizophrenia. This can be accounted for by other psychiatric
disorders whereby elevated dopamine levels are seen only when psychosis is
present. 

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