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Neurons that use the transmitter dopamine are thought either to fire too often, or to send too much information.
It is thought that an excess of dopamine in particular brain regions can be related to certain symptoms.
For example, such an increase in the Broca’s region (responsible for formation of language) can impair logical speech, a classic symptom of schizophrenia.
Evidence to support this theory comes from drug trials involving those with schizophrenia and those without the disorder.
Drugs that increase dopamine levels (amphetamine and cocaine) are correlated with hallucinations and delusions.
Patients with Parkinson’s disease are often treated with a synthetic form of dopamine called L-dopa. If their dosage is too high, it also creates symptoms in these individuals identical to those in people with schizophrenia, such as hallucinations.
Post mortem studies, brain scans and autopsies have shown that schizophrenic patients have larger number of dopamine receptors than usual.
Wise et al. (1974) found that brain fluid from deceased patients had abnormally low levels of the enzyme which breaks down dopamine, suggesting it may have been present in excessive quantities.
Positron emission tomography (PET) scan analysis of dopamine usage indicates a greater number of receptors in the striatum, limbic system and cortex of the brain in those with schizophrenia than in those without.
Excessive dopamine activity in these areas may be linked to positive symptoms.
Nestler, 1997 suggests that decreased dopamine activity in the prefrontal cortex of schizophrenia patients may correlate with negative symptoms such as flattened affect.
