The extent to which is can be

The third iteration
of the Dopamine Hypothesis of Schizophrenia makes reference to the theory that schizophrenic
symptoms are caused by pre synaptic hyper dopaminergic signalling due to
potential risk factors (Howes and Kapur, 2009). There is a broad consensus that
the dopamine hypothesis has contributed to a significant understanding of the
underlying mechanisms of schizophrenia due to dopaminergic dysregulation in
specific pre frontal brain regions (Brisch et al., 2014). It should be acknowledged that schizophrenia
is not solely psychotic. Negative and cognitive deficits need be taken into
account in regards to hyper dopaminergic states to comprehend the disorder it its
entirety, as both 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. This essay will consider an array of evidence
to disregard these accusations and acknowledge the extent to which excessive
dopamine affects the onset of schizophrenic symptoms. Albeit 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 suggesting dopamine activity may be controlled through
this neurotransmitter.