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Part of the book series: NATO ASI Series ((ASHT,volume 51))

Abstract

The dopamine hypothesis for the pathophysiology of schizophrenia states that the schizophrenic symptoms are related to an overactivity in central dopaminergic transmission [1]. This hypothesis was stimulated by the hypothesis for antipsychotic drug action which postulates that the antipsychotic effect is mediated by a blockade of dopamine receptors [2]. Further, the psychotic symptoms induced by the dopamine releasing agent amphetamine resemble those of paranoid schizophrenia [3]. Later the dopamine hypothesis for schizophrenia was supported by post-mortem studies of brains from schizophrenic patients by the finding of an increased density of D2 dopamine receptors in the basal ganglia [4]. Some studies have reported increased densities only in patients who were maintained on neuroleptic drug treatment until the time of death indicating that the increase in D2 receptor density rather is induced by neuroleptic drug treatment.

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Nordström, AL. (1998). PET Studies of the Dopamine Hypotheses in Schizophrenia. In: Gulyás, B., Müller-Gärtner, H.W. (eds) Positron Emission Tomography: A Critical Assessment of Recent Trends. NATO ASI Series, vol 51. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-4996-9_21

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  • DOI: https://doi.org/10.1007/978-94-011-4996-9_21

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