The refers to the theory that schizophrenic symptoms are

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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The Dopamine
Hypothesis III considers an array of complex factors linking both environmental
and biological aspects that affect dopamine regulation in the presynaptic dopamine
striatal. Thus accounting for individual differences in genetic predispositions
and sociocultural factors such as stress and trauma. Presynaptic hyper dopaminergic
functioning is critical to understanding how particular symptoms arise in schizophrenia.

Although dopamine activity cannot be explicitly measured, radiotracers of brain
images allow us to assess presynaptic dopamine functioning. Evidence has found
that presynaptic dopamine functioning is elevated in individuals with
schizophrenia, and has been linked to the onset of psychosis. Findings have
found that in 7 out of 9 studies elevated dopamine in presynaptic striatum was
found in those with schizophrenia. The use of fluorodopa radiotracers enables
us to study over-activity of dopamine in the brain with results implying that
in both medicated and unmediated schizophrenics, dopamine functioning is seen
in the pre synaptic (McGowan et al, 2004). This suggests that by decreasing
dopamine in the presynaptic striatum, psychotic symptoms would be reduced. However,
an interesting factor that should be taken into consideration when looking at
research into presynaptic dopamine functioning is whether the individual is
stable or relapsing from the disorder. These different states may cause
presynaptic dopamine functioning to alter, potentially influencing the results.

By acknowledging this, research into these differences as these findings would
have important implications on treatments (Laruelle, Abi-Dargham, 1999).

 

Contradicting
results using PET studies found no differences in striatal dopaminergic
synapses between 147 healthy controls and 202 schizophrenic individuals, therefore
suggesting that alterations in the striatum are not needed for the onset of
psychotic symptoms (Fusar-Poli and Meyer-Lindenberg, 2013). There results
however concentrated on dopamine active transporters in the synapse suggesting why
there may be differences in the data. Research into this area is relatively
new, suggesting further investigation is needed to come to a conclusive judgement
in relation to DAT and presynaptic functioning. This being said, psychosis is
not explicit to schizophrenia, and is seen in other disorders implying that dopamine
dysregulation may increase vulnerability to psychotic symptoms (Van Os et al.,
2008). However, by taking this into account it is clear that heightened
dopaminergic functioning leads to the onset of psychosis, giving clear
explanation into the use of antipsychotics. Furthermore, Howes and Kapur (2009)
found an abnormally large number of D2/D3 receptors in individuals with
schizophrenia which is a 10-20 percent increase when compared to a healthy
control group. This indicates that an increase in dopamine sensitivity may be
due to larger quantity of synaptic receptors, thus in turn increasing dopamine
transmission. Vivo imaging studies indicate blocking D2 receptors are vital in
controlling psychotic symptoms through the use of antipsychotics.