The thirdversion of the Dopamine Hypothesis of Schizophrenia refers to the theory that schizophrenicsymptoms are caused by pre synaptic hyper dopaminergic signalling due topotential risk factors. Literature agrees that thedopamine hypothesis has contributed to a significant understanding of theunderlying mechanisms of schizophrenia due dopaminergic dysregulation inspecific pre frontal brain regions (Brisch et al.
, 2014). It is important to understandthat schizophrenia is more than a state of psychosis, as both negative andcognitive symptoms link to poor quality of life, and an inability to function (Lin et al., 2013). Howes and Kapur (2009) acknowledgethat the Dopamine Hypothesis III gravitates towards “psychosis – in –schizophrenia” (p.556), potentially limiting the extent to which is can beapplied to every aspect of schizophrenia. However, throughout this essay new evidencewill be considered in order to disregard these accusations and acknowledge theextent to which excessive dopamine affects the onset of schizophrenic symptoms.
Even though there is strong evidence of the role of dopamine, it fails to acknowledge what may be influencing abnormal dopamine levels. Glutamatehas been found to regulate dopamine synthesise through NMDAR receptors givingexplanation into how dopamine activity may be regulated through thisneurotransmitter.