Unit on Integrative Neuroimaging, National Institute of Mental Health, 9000 Rockville Pike, Bethesda, MD 20892-1365, United States
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Bennett, M. R., Monoaminergic synapses and schizophrenia: 45 Years of neuroleptics (1998) J. Psychopharmacol., 12, pp. 289-30
Lewis, D. A., Anderson, S. A., The functional architecture of the prefrontal cortex and schizophrenia (1995) Psychol. Med., 25, pp. 897-994
Jaskiw, G. E., Karoum, F. K., Weinberger, D. R., Persistent elevations in dopamine and its metabolites in the nucleus accumbens after mild subchronic stress in rats with ibotenic acid lesions of the medial prefrontal cortex (1990) Brain. Res., 534, pp. 321-323
Pycock, C. J., Kerwin, R. W., Carter, C. J., Effect of lesion of cortical dopamine terminals on subcortical dopamine receptors in rats (1980) Nature, 286, pp. 74-76
Weinberger, D. R., Implications of normal brain development for the pathogenesis of schizophrenia (1987) Arch. Gen. Psychiatry, 44, pp. 660-669
Grace, A. A., Cortical regulation of subcortical dopamine systems and its possible relevance to schizophrenia (1993) J. Neural Transm. Gen. Sect., 91, pp. 111-134
Deutch, A. Y., The regulation of subcortical dopamine systems by the prefrontal cortex: Interactions of central dopamine systems and the pathogenesis of schizophrenia (1992) J. Neural Transm. Suppl., 36, pp. 61-89
Lindstrom, L. H., Increased dopamine synthesis rate in medial prefrontal cortex and striatum in schizophrenia indicated by L- (-11C) DOPA and PET (1999) Biol. Psychiatry, 46, pp. 681-688
Dao-Castellana, M. H., Presynaptic dopaminergic function in the striatum of schizophrenic patients (1997) Schizophr. Res., 23, pp. 167-174
Elkashef, A. M., 6- (18) F-DOPA PET study in patients with schizophrenia. Positron emission tomography (2000) Psychiatry Res., 100, pp. 1-11
Wong, D. F., Positron emission tomography reveals elevated D2 dopamine receptors in drug-naive schizophrenics (1986) Science, 234, pp. 1558-1563
Jackson, M. E., Frost, A. S., Moghaddam, B., Stimulation of prefrontal cortex at physiologically relevant frequencies inhibits dopamine release in the nucleus accumbens (2001) J. Neurochern., 78, pp. 920-923
Christie, M. J., Bridge, S., James, L. B., Beart, P. M., Excitotoxin lesions suggest an aspartatergic projection from rat medial prefrontal cortex to ventral tegmental area (1985) Brain Res., 333, pp. 169-172
Kegeles, L. S., Modulation of amphetamine-induced striatal dopamine release by ketamine in humans: Implications for schizophrenia (2000) Biol. Psychiatry, 48, pp. 627-640
Carr, D. B., Sesack, S. R., Projections from the rat prefrontal cortex to the ventral tegmental area: Target specificity in the synaptic associations with mesoaccumbens and mesocortical neurons (2000) J. Neurosci., 20, pp. 3864-3873
Saunders, R. C., Kolachana, B. S., Bachevalier, J., Weinberger, D. R., Neonatal lesions of the medial temporal lobe disrupt prefrontal cortical regulation of striatal dopamine (1998) Nature, 393, pp. 169-171
Swerdlow, N. R., Geyer, M. A., Using an animal model of deficient sensorimotor gating to study the pathophysiology and new treatments of schizophrenia (1998) Schizophr. Bull., 24, pp. 285-301
Grace, A. A., Phasic versus tonic dopamine release and the modulation of dopamine system responsivity: A hypothesis for the etiology of schizophrenia (1991) Neuroscience, 41, pp. 1-24
Daniel, D. G., The effect of amphetamine on regional cerebral blood flow during cognitive activation in schizophrenia (1991) J. Neurosci., 11, pp. 1907-1917
Napier, T. C., Chrobak, J. J., Evaluations of ventral pallidal dopamine receptor activation in behaving rats (1992) Neuroreport, 3, pp. 609-611
Goldman-Rakic, P. S., The physiological approach: Functional architecture of working memory and disordered cognition in schizophrenia (1999) Biol. Psychiatry, 46, pp. 650-661
(1987) Diagnostic and Statistical Manual of Mental Disorders: DSM-III-R, , American Psychiatric Association, Washington, DC
Miletich, R. S., 6- [18F] fluoro-L-dihydroxyphenylalanine metabolism and positron emission tomography after catechol-O-methyltransferase inhibition in normal and hemiparkinsonian monkeys (1993) Brain Res., 626, pp. 1-13
Berman, K. F., Physiological activation of a cortical network during performance of the Wisconsin Card Sorting Test: A positron emission tomography study (1995) Neuropsychologia, 33, pp. 1027-1046
Woods, R. P., Mazziotta, J. C., Cherry, S. R., MRI-PET registration with automated algorithm (1993) J. Comput. Assist. Tomogr., 17, pp. 536-546
Brooks, D. J., Differing patterns of striatal 18F-dopa uptake in Parkinson's disease, multiple system atrophy, and progressive supranuclear palsy (1990) Ann. Neurol., 28, pp. 547-555
Patlak, C. S., Blasberg, R. G., Fenstermacher, J. D., Graphical evaluation of blood-to-brain transfer constants from multiple-time uptake data (1983) J. Cereb. Blood Flow Metab., 3, pp. 1-7
Reduced prefrontal activity predicts exaggerated striatal dopaminergic function in schizophrenia
Both dopaminergic neurotransmission and prefrontal cortex (PFC) function are known to be abnormal in schizophrenia. To test the hypothesis that these phenomena are related, we measured presynaptic dopaminergic function simultaneously with regional cerebral blood flow during the Wisconsin Card Sorting Test (WCST) and a control task in unmedicated schizophrenic subjects and matched controls. We show that the dopaminergic uptake constant Ki in the striatum was significantly higher for patients than for controls. Patients had significantly less WCST-related activation in PFC. The two parameters were strongly linked in patients, but not controls. The tight within-patient coupling of these values, with decreased PFC activation predicting exaggerated striatal 6-fluorodopa uptake, supports the hypothesis that prefrontal cortex dysfunction may lead to dopaminergic transmission abnormalities.
Reduced prefrontal activity predicts exaggerated striatal dopaminergic function in schizophrenia
No results.
Reduced prefrontal activity predicts exaggerated striatal dopaminergic function in schizophrenia
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