Abstract

The dopamine hypothesis is widely believed to be an attractive explanation for a variety of symptoms of schizophrenic patients. Paranoid behavior and tardive dyskinesia are the most prominent symptoms which have been related to dopaminergic overactivity. While presynaptic activity with increased synthesis or release of dopamine (DA) might contribute to this functional state of the DA-neuron, measurement of postsynaptic receptor function by radiolabelled neuroleptic drugs has been used to define more precisely the functional significance of sub- and supersensitive receptors. Positive symptoms defined as hallucinations, delusions and formal thought disorder were positively correlated with increased spiperone binding sites in post mortem human putamen of schizophrenics while there was no significance to negative symptoms (Owen et al, 1981). Although neuroleptic drug treatment might have contributed to an increase in binding number as shown in animal studies and human post mortem analysis (Seeman, 1980) in a certain subgroup of schizophrenics an endogenous overstimulation of postsynaptic receptors as pathogenic cause of specific symptoms might occur. It is, however, very unlikely to assume that a single and localized disturbance contributes to such a heterogenous complex of symptoms (or diseases) like schizophrenia. Therefore, we have tried to characterize the human post mortem brain tissue with regard to clinical and biochemical criteria.

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