Effects of the D-1 Agonist SKF-38393 Combined With Haloperidol in Schizophrenic Patients
- 1 February 1990
- journal article
- research article
- Published by American Medical Association (AMA) in Archives of General Psychiatry
- Vol. 47 (2), 190-191
- https://doi.org/10.1001/archpsyc.1990.01810140090014
Abstract
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.2 Animal 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 cortexKeywords
This publication has 4 references indexed in Scilit:
- Implications of Normal Brain Development for the Pathogenesis of SchizophreniaArchives of General Psychiatry, 1987
- PET analysis of human dopamine receptor subtypes using 11C-SCH 23390 and 11C-raclopridePsychopharmacology, 1987
- Oral dyskinesia in rats following brain lesions and neuroleptic drug administrationPsychopharmacology, 1982
- Effect of lesion of cortical dopamine terminals on subcortical dopamine receptors in ratsNature, 1980