The Dopamine
Hypothesis III acknowledges that the driving force of schizophrenia is due to
multiple pathways that lead to excessive presynaptic hyper dopaminergic functioning,
however
it fails to recognise what regulates dopamine behaviour. Dopamine synthesis has
been linked to faulty glutamate NMDAR receptors giving a clearer indication
into how dopamine levels are fluctuated. The fact that antipsychotic drugs only
block D2 receptors with at least 30% of individuals failing to respond to
medication indicates that other mechanisms currently not targeted are a result
of the initial problems not being treated. In order to study the effects of
glutamate on schizophrenia, HMRS and PET imaging have been used.  Dopamine regulation is sensitive towards
glutamate, indicating that changes in glutamate levels by blocking NMDAR
receptors mediates dopamine activity. By doing so it puts a wider understanding
of how dopamine is regulated in the pre frontal cortex and hippocampus. Studies
using ketamine have been of particular interest as the drug blocks the NMDAR
receptor causing dysregulation of glutamate leading to an increased sensitivity
of dopamine. Poels et al (2013) found that in healthy controls when given
ketamine there was an NMDAR blockade on striatal dopamine release leading to
similar cognitive impairments, negative and positive symptoms likewise to those
seen in schizophrenia (Coyle, 2006). As a result, supports that dopamine
regulation should be targeted further downstream at the NMDAR to reduce
schizophrenic symptoms by increasing activity at their sites, to benefit those
who are unable to respond to antipsychotics. While research is plausible, there
are limitations when using H-MRS. Although a popular technique used in
schizophrenia they are not able to distinguish between intra or extracellular
compartments, limiting how specific the results are. Radiotracers are far abler
to give insight into specific areas, indicating that future research should
focus on these techniques in order to strengthen the data to further understand
this complex system. Individuals may be more sensitive to glutamate deficiency,
implying that these mechanisms must be targeted to control dopamine functioning
if individual does not respond to antipsychotics.   

 

Although the
dopamine hypothesis III seems plausible, negative symptoms and cognitive
deficits need to be accounted for more widely. As the hypothesis has been re-worked
throughout the years, this is most likely going to happen in the future as techniques
are enhanced leading to more accurate results.  However, by accepting the role of dopamine as
the biggest contributor to the onset of schizophrenia, it is easy to rationalize
the use of drugs such as antipsychotics to treat positive symptoms (Read, Mosher
and Bentall, 2005). It is hard to imagine schizophrenia diagnosed and treated
without dopamine at the forefront, due to its response to antipsychotics in dampening
its effects giving great accountability to the neurochemical imbalance in the
brain. Nevertheless, as there are a several individuals’ who are
treatment-resistant, this leaves many individuals still suffering with positive
symptoms, and the majority still unable to reach full benefits due to their
persistent negative and cognitive symptoms (Lally et al., 2016). However, by
taking into account different aspects of the dopamine hypothesis III and dopamine
sensitivity due to NMDAR receptors, it enables us to target different stages of
the illness by using a selection of treatments. Overall, dopamine can be
described as the driving force of schizophrenia, and acknowledging its
interactions with risk factors to schizophrenic symptoms will only strengthen research.

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