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Effects of the D-1 Agonist SKF-38393 Combined With Haloperidol in Schizophrenic Patients

Michael Davidson, MD; Phil D. Harvey, PhD; R. Lindsey Bergman; Peter Powchik, MD; Rami Kaminsky, MD; Miklos F. Losonczy, PhD, MD; Kenneth L. Davis, MD
Arch Gen Psychiatry. 1990;47(2):190-191. doi:10.1001/archpsyc.1990.01810140090014.
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To the Editor.—  The original dopamine (DA) hypothesis of schizophrenia suggested that D-2 receptor densities are augmented in subcortical brain areas and that the therapeutic effects of antipsychotic drugs are mediated by the antidopaminergic properties of these drugs. However, the notion that augmented dopaminergic activity is a consistent and pervasive phenomenon in schizophrenic patients is probably too simplistic. More recent elaboration of the DA hypothesis suggests that, depending on the brain area, dopaminergic activity could be increased or decreased.1 In fact, clinical observations attribute some schizophrenic symptoms to frontal cortical dopaminergic deficits, and cerebral blood flow studies in schizophrenic patients indicate that frontal DA activity is reduced rather than augmented.2Animal experiments support the notion that reduced dopaminergic activity in cortical brain regions can coexist with, or even be the cause of, increased dopaminergic activity in subcortical areas. Lesions of dopaminergic innervation of the medial prefrontal cortex


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