Abstract
The introduction of chlorpromazine in psychiatry (Delay and Deniker 1952) demonstrated that acute schizophrenic symptoms can successfully be treated with drugs, and this finding stimulated the search for the pathophysiological and pathobiochemical changes underlying schizophrenia. Steck (1954) and Haase (1955) first described extrapyramidal symptoms and drug-induced parkinsonism as possible side-effects occurring during treatment with neuroleptic agents. The investigation of dopamine as a neurotransmitter (Carlsson et al. 1958; Carlsson and Lindqvist 1963), the dopaminergic deficit in the basal ganglia of patients suffering from Parkinson’s disease (Ehringer and Hornykiewicz 1960) as a result of the degeneration of nigral dopaminergic cells (Hornykiewicz 1973) and the efficacy of L-dopa in the treatment of parkinsonism, especially of akinesia (Birkmayer and Hornykiewicz 1962), led to the hypothesis that dopamine antagonism was responsible for both anti-psychotic and extrapyramidal effects of neuroleptics. The “dopamine hypothesis” of schizophrenia supposes that a functional overactivity of dopaminergic neurotransmission results in acute schizophrenic symptoms (van Rossum 1966; Meltzer and Stahl 1976). According to the positive symptoms appearing during an acute episode of schizophrenia, on the biochemical level an overstimulation of postsynaptic dopamine receptors in the mesolimbic and mesocortical projection areas is hypothesised. The efficacy of classic neuroleptic agents is explained by their ability to block post-synaptic dopamine receptors ofthe D2 type.
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Klimke, A., Klieser, E. (1991). The Treatment of Positive and Negative Schizophrenic Symptoms with Dopamine Agonists. In: Marneros, A., Andreasen, N.C., Tsuang, M.T. (eds) Negative Versus Positive Schizophrenia. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-76841-5_23
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