Contradicting to schizophrenia, and is seen in other

results using PET studies found no differences in striatal dopaminergic
synapses between 147 healthy controls and 202 schizophrenic individuals, therefore
suggesting that alterations in the striatum are not needed for the onset of
psychotic symptoms (Fusar-Poli and Meyer-Lindenberg, 2013). There results
however concentrated on dopamine active transporters in the synapse suggesting why
there may be differences in the data. Research into this area is relatively
new, suggesting further investigation is needed to come to a conclusive judgement
in relation to DAT and presynaptic functioning. This being said, psychosis is
not explicit to schizophrenia, and is seen in other disorders implying that dopamine
dysregulation may increase vulnerability to psychotic symptoms (Van Os et al.,
2008). However, by taking this into account it is clear that heightened
dopaminergic functioning leads to the onset of psychosis, giving clear
explanation into the use of antipsychotics. Furthermore, Howes and Kapur (2009)
found an abnormally large number of D2/D3 receptors in individuals with
schizophrenia which is a 10-20 percent increase when compared 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. Vivo imaging studies indicate blocking D2 receptors are vital in
controlling psychotic symptoms through the use of antipsychotics.


It is important
to acknowledge all aspects of schizophrenia in terms of effective treatments.

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Most research tends to focus solely on the role of D2 receptors to account for psychotic
symptoms. However, by acknowledging an array of receptors, we are able to
account for negative and cognitive deficits due to D1 dysfunction (Howes and
Kapur, 2009).  PET scans have been used
to study dopamine depletion in the prefrontal cortex, whereby changes in the d1PFCn
has shown to cause negative symptoms and cognitive deficits. This suggests that
the d1PFC has an impact on the symptoms seen in schizophrenic patients due to
the insufficient signalling between D1 receptors (Goldman-Rakic et al., 2004).  Research suggests that treatment must also
target D1 receptors in order to lower cognitive deficits to restore cognitive
functioning in schizophrenic patients (Tamminga, 2006). These results indicate
that the array of symptoms need to be targeted and treated separately for patients
to recover. Findings have found by targeting D1 receptors with D1 agonists they
are able to alleviate cognitive deficits as D1 agonists are able to enhance the
receptors signalling, thus suggesting that dysfunction of the D1 receptor can
cause these cognitive deficits (Goldman-Rakic et al., 2004). The use of antipsychotics and
D1 agonists have shown to increase the efficacy of working memory and the
efficiency of D1/D2 receptors, indicating that an array of treatments should be
used in order to regulate the range of symptoms associated with schizophrenia (Kim et al., 2015). Further
research is needed to analyse the effectiveness of D1 agonists in the treatment
of schizophrenia, and the associated long term effects in order to better understand
the contribution of D1 receptors in the development of schizophrenia. Although the emergence of theories that acknowledge dopamine receptors
and dopamine deregulation have received great support, they fail to recognise the
cause of these symptoms. 


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