Dopamine and Schizophrenia

Dopamine and Schizophrenia
This hypothesis postulates that dopamine (D2) receptor neurotransmission
hyperactivity in limbic and subcortical areas leads to positive schizophrenia symptoms. On the
other hand, negative and cognitive schizophrenia symptoms may be attributed to dopamine D1
receptor neurotransmission hypo-functionality in the prefrontal cortex. Studies that support this
have indicated increased dopamine D2 receptor density in schizophrenia sufferers’ post-
mortem brain tissue. Also, D2 receptors upregulation in schizophrenic patients’ caudate
nucleus correlates directly with poor performance in cognitive tasks that involve corticosteroid
pathways (Desbonnet). In cerebral spinal fluid samples, patients who have schizophrenia are
found to have high homovanillic acid levels. Homovanillic acid is a product that results from
the breakdown of dopamine. Amphetamine and other dopamine-releasing drugs apart from
having a D2- antagonist property also has psychotomimetic properties that are common to most
of the antipsychotic treatments prescribed currently, which gives evidence to dopamine
hypothesis of schizophrenia.
Works Cited
Desbonnet, Lieve. "Modeling the Psychopathological Dimensions of Schizophrenia."
Handbook of Behavioral Neuroscience, Elsevier, 2016.

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