Abstract

The binding of [ 3H]paroxetine and [ 3H]ketanserin to particulate membranes from frontal cortex of subjects who had or did not have schizophrenia was measured as was [ 3H]paroxetine binding to particulate membranes from the hippocampus and caudate nucleus. There was no change in either the affinity or density of [ 3H]ketanserin binding to membranes from the frontal cortex of subjects who had schizophrenia. Similarly, there was no difference in the density of [ 3H]paroxetine binding to membranes from subjects who had or did not have schizophrenia. The affinity of [ 3H]paroxetine binding in the frontal cortex and putamen did not differ in subjects who had schizophrenia. By contrast, there was a significant decrease in the affinity of [ 3H]paroxetine binding to the hippocampal membrane from subjects who had schizophrenia (0.40 ± 0.06 nM vs 0.26 ± 0.02 nM; p < 0.05). Furthermore, this difference was more apparent in the subjects who had schizophrenia and committed suicide (0.49 ± 0.09 nM) than it was in those who had schizophrenia but did not commit suicide (0.32 ± 0.09 nM). As [ 3H]ketanserin binds to the serotonin 2 receptor our data suggest that this receptor is not changed in the Brodmann's area 9 of the frontal cortex. By contrast, [ 3H]paroxetine binds to the serotonin transporter and therefore our data suggest that the serotonin transporter is altered in the hippocampus of subjects with schizophrenia.

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