The third
version of the Dopamine Hypothesis of Schizophrenia refers to the theory that schizophrenic
symptoms are caused by pre synaptic hyper dopaminergic signalling due to
potential risk factors. 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). It is important to understand
that schizophrenia is more than a state of psychosis, as both negative and
cognitive symptoms link to poor quality of life, and an inability to function (Lin et al., 2013). Howes and Kapur (2009) acknowledge
that the Dopamine Hypothesis III gravitates towards “psychosis – in –
schizophrenia” (p.556), potentially limiting the extent to which is can be
applied to every aspect of schizophrenia. However, throughout this essay new evidence
will be considered in order to disregard these accusations and acknowledge the
extent 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. Glutamate
has been found to regulate dopamine synthesise through NMDAR receptors giving
explanation into how dopamine activity may be regulated through this
neurotransmitter. 

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