Contradictingresults using PET studies found no differences in striatal dopaminergicsynapses between 147 healthy controls and 202 schizophrenic individuals, thereforesuggesting that alterations in the striatum are not needed for the onset ofpsychotic symptoms (Fusar-Poli and Meyer-Lindenberg, 2013). There resultshowever concentrated on dopamine active transporters in the synapse suggesting whythere may be differences in the data. Research into this area is relativelynew, suggesting further investigation is needed to come to a conclusive judgementin relation to DAT and presynaptic functioning.
This being said, psychosis isnot explicit to schizophrenia, and is seen in other disorders implying that dopaminedysregulation may increase vulnerability to psychotic symptoms (Van Os et al.,2008). However, by taking this into account it is clear that heighteneddopaminergic functioning leads to the onset of psychosis, giving clearexplanation into the use of antipsychotics.
Furthermore, Howes and Kapur (2009)found an abnormally large number of D2/D3 receptors in individuals withschizophrenia which is a 10-20 percent increase when compared to a healthycontrol group. This indicates that an increase in dopamine sensitivity may bedue to larger quantity of synaptic receptors, thus in turn increasing dopaminetransmission. Vivo imaging studies indicate blocking D2 receptors are vital incontrolling psychotic symptoms through the use of antipsychotics. It is importantto acknowledge all aspects of schizophrenia in terms of effective treatments.
Most research tends to focus solely on the role of D2 receptors to account for psychoticsymptoms. However, by acknowledging an array of receptors, we are able toaccount for negative and cognitive deficits due to D1 dysfunction (Howes andKapur, 2009). PET scans have been usedto study dopamine depletion in the prefrontal cortex, whereby changes in the d1PFCnhas shown to cause negative symptoms and cognitive deficits. This suggests thatthe d1PFC has an impact on the symptoms seen in schizophrenic patients due tothe insufficient signalling between D1 receptors (Goldman-Rakic et al., 2004).
Research suggests that treatment must alsotarget D1 receptors in order to lower cognitive deficits to restore cognitivefunctioning in schizophrenic patients (Tamminga, 2006). These results indicatethat the array of symptoms need to be targeted and treated separately for patientsto recover. Findings have found by targeting D1 receptors with D1 agonists theyare able to alleviate cognitive deficits as D1 agonists are able to enhance thereceptors signalling, thus suggesting that dysfunction of the D1 receptor cancause these cognitive deficits (Goldman-Rakic et al., 2004). The use of antipsychotics andD1 agonists have shown to increase the efficacy of working memory and theefficiency of D1/D2 receptors, indicating that an array of treatments should beused in order to regulate the range of symptoms associated with schizophrenia (Kim et al.
, 2015). Furtherresearch is needed to analyse the effectiveness of D1 agonists in the treatmentof schizophrenia, and the associated long term effects in order to better understandthe contribution of D1 receptors in the development of schizophrenia. Although the emergence of theories that acknowledge dopamine receptorsand dopamine deregulation have received great support, they fail to recognise thecause of these symptoms.