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The role of limbic and cortical regions in schizophrenia: Focus on dopamine

Published online by Cambridge University Press:  16 April 2020

G. Marchese  and
L. Pani
G. Marchese
Affiliation:
C.N.R. Institute for Neurogenetics and Neuropharmacology and Neuroscienze Scarl, Via Palabanda, 9, 09124Cagliari, Italy
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Summary

Dopamine is implicated in the pathogenesis of both the positive and the negative symptoms of schizophrenia. Clinical efficacy of antipsychotic drugs, without the production of side-effects, may be achieved by a dose–response separation of pharmacological function, regional (i.e., anatomical) selectivity of action, or by the selective targeting of neuroreceptors. The atypical antipsychotics have many different ways of acting on receptors in the brain, but they have in common a decreased likelihood of producing extrapyramidal side-effects. Patients respond well to them by showing improvements of both positive and negative symptoms. The preclinical profile of amisulpride shows specificity for D2/D3 dopamine receptors and selective activity in the limbic system. There is evidence that amisulpride is effective in treating both the negative and positive symptoms of schizophrenia, and that it has a low propensity to induce motor side-effects. Therefore, both positive and negative symptoms can be treated, without inducing these side-effects, by selectively targeting dopamine receptors.

Keywords

SchizophreniaDopamineLimbic systemCerebral cortex
Type
Research Article
Information
European Psychiatry , Volume 17 , Issue S4: Mind Matters - International Schizophrenia Forum , August 2002 , pp. 349s - 354s
Copyright
Copyright Éditions scientifiques et médicales Elsevier SAS 2002

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References

Carlsson, A.The dopamine theory revisited. In: Hirsch, SRWeinberger, DR Eds. Schizophrenia. Oxford: Blackwell Science; 1995. p. 379–400.Google ScholarPubMed
Cudennec, AFage, DBénavidès, JScatton, B.Effects of amisulpride, an atypical antipsychotic which blocks presynaptic dopamine autoreceptors, on integrated functional cerebral activity in the rat. Brain Research 1997;768:257–65.CrossRefGoogle ScholarPubMed
Gaddum, Sir. The Ciba Symposium on Monoamines. 1961.Google Scholar
Goldman-Rakic, PSMuly EC, IIIWilliams, GV.D1 receptors in prefrontal cells and circuits. Brain Res Brain Res Rev 2000 Mar;31:295–301.CrossRefGoogle ScholarPubMed
Hornykiewicz, O.Dopamine (3–hydroxytyramine) and brain function. Pharmacol Rev 1966;18:925–64.Google ScholarPubMed
Knable, MBWeinberger, DR.Dopamine, the prefrontal cortex and schizophrenia. J Psychopharmacol 1997;11:123–31.CrossRefGoogle Scholar
Laruelle, MAbi-Dargham, Avan Dyck, CHGil, RD’Souza, CDErdos, J et al. Single photon emission computerized tomography imaging of amphetamine–induced dopamine release in drug free schizophrenic patients. Proc Natl Acad Sci USA 1996;93:9235–40.CrossRefGoogle Scholar
Xiberas, XMartinot, JLMallet, LArtiges, ECanal, MLoc’h, C et al. In vivo extrastriatal and striatal D2 dopamine receptor blockade by amisulpride in schizophrenia. J Clin Psychopharmacol 2001;21:207–14.CrossRefGoogle Scholar
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