There is avast amount of evidence to support the dopamine hypothesis III in explainingschizophrenia. However, evidence is inconsistent to the extent it plays a rolein the onset of schizophrenia, and how all the individual aspects of thehypothesis may link to its development. One of the main symptoms that has been focused on is psychosis, whichdopamine has consistently been linked to, thus makingit easier to account for the positive symptoms (McKenna, 2013), than it does for negative andcognitive symptoms (Kapur, 2003).

 Vivo imaging studies has alloweddopaminergic functioning to be assessed in the pre synaptic, leading away fromthe idea that the disorder is due to elevations in D2 receptors (Kambeitz et al., 2013). Findings have supported the latest hypothesis in that dopaminedysregulation occurs further upstream in the presynaptic system, which explainswhy when apatient stops taking antipsychotics the symptoms come back almost instantaneously,thus indicating that there are many factors that need to be held accountable. However,research on antipsychotics have been at the forefront of treating schizophreniathat dopamine must not be disregarded in order to understand psychosis.However, it fails to acknowledge what may be driving these alterations indopamine, therefore indicating that other neurotransmitters such as glutamate dysfunctionmust be taken into account to explain these changes.  

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