Abstract
The last three decades of research in biochemical psychiatry have been characterized by many efforts to prove the dopamine (DA) hypothesis of schizophrenia in connection with the effect and supposed mechanism of action of neuroleptic drugs (NLs) (Matthysee 1973). This hypothesis was sustained by clinical results, both by the exacerbating effect of DA agonists such as L-dopa and amphetamine and by the antipsychotic effect of neuroleptic drugs, for (review see Ackenheil et al. 1980). However, these clinical effects are restricted to certain symptoms of schizophrenia and nosological subcategories and, in general, only productive symptoms and the paranoid hallucinatoric type of schizophrenia are involved, whereas minus symptoms and the hebephrenic type or the schizophrenia simplex type interact with these substances to a lower extent. Biochemical studies more or less failed to prove this hypothesis. The progress of neuroendocrinological research strategies and of knowledge of receptor measurements promises a better understanding of the pathophysiology of schizophrenia.
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Ackenheil, M., Albus, M., Bondy, B., Müller-Spahn, F., Münch, U., Naber, D. (1985). Biochemical and Neuroendocrine Studies in Schizophrenics: Attempts to Characterize the Illness Biochemically. In: Beckmann, H., Riederer, P. (eds) Pathochemical Markers in Major Psychoses. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-69743-2_9
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DOI: https://doi.org/10.1007/978-3-642-69743-2_9
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