There is a
vast amount of evidence to support the dopamine hypothesis III in explaining
schizophrenia. However, evidence is inconsistent to the extent it plays a role
in the onset of schizophrenia, and how all the individual aspects of the
hypothesis may link to its development. 
One of the main symptoms that has been focused on is psychosis, which
dopamine has consistently been linked to, thus making
it easier to account for the positive symptoms (McKenna, 2013), than it does for negative and
cognitive symptoms (Kapur, 2003). Vivo imaging studies has allowed
dopaminergic functioning to be assessed in the pre synaptic, leading away from
the idea that the disorder is due to elevations in D2 receptors (Kambeitz et al., 2013). Findings have supported the latest hypothesis in that dopamine
dysregulation occurs further upstream in the presynaptic system, which explains
why when a
patient stops taking antipsychotics the symptoms come back almost instantaneously,
thus indicating that there are many factors that need to be held accountable. However,
research on antipsychotics have been at the forefront of treating schizophrenia
that dopamine must not be disregarded in order to understand psychosis.

However, it fails to acknowledge what may be driving these alterations in
dopamine, therefore indicating that other neurotransmitters such as glutamate dysfunction
must be taken into account to explain these changes.  

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