The efficacy of antipsychotic drugs, which traditionally worked through the dopaminergic system, has been the major stimulus driving the "dopamine hypothesis" of schizophrenia (Willner, 1997). The evidence that antipsychotic drugs all share the ability to block dopamine receptors led to the concept that overactivity in some subcortical dopamine cells causes psychotic symptoms such as hallucinations, delusions, and disorganized thought and behavior. A more recent modification of this theory suggests that hypofunction of dopamine in the mesocortical dopamine neurons is responsible for negative symptoms such as blunted affect and poverty of speech.
The formidable evidence that antipsychotic drugs work at least in large part because they block dopamine receptors does not necessarily mean that people with schizophrenia have abnormal dopamine transmission. However, other evidence also suggests there is an abnormality in the dopamine system. For instance, dopamine agonists such as amphetamines and methylphenidate worsen the psychotic symptoms of schizophrenia, and some studies of dopamine function in living patients (using such methods as PET) have also revealed an abnormality in dopamine transmission.
Nonetheless, there are important limitations to the dopamine theory. First, blocking dopamine receptors does not resolve all psychotic symptoms; despite taking high doses of such medications, some patients' psychotic symptoms improve little. Moreover, these drugs do not improve other aspects of schizophrenia, such as the cognitive impairment or the blunted affect and poverty of speech. No one neurotransmitter can explain the widespread problems found in schizophrenia, and there is a great deal of evidence that other neurotransmitters are also abnormal in this disorder.
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