The effect on human monoamine oxidase activity of subcutaneous injections of adrenaline.
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Biomedical subjects
Publications and source records attributed to F Owen.
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Elevated blood serotonin, perhaps secondary to reduced platelet MAO, has been reported in a group of chronic schizophrenic patients. We have failed to find elevated platelet serotonin, or any relationship between platelet serotonin and MAO either in a group of unmedicated chronic schizophrenic patients or in a group of schizoaffective patients. Possible reasons for these discrepancies are discussed.
Platelet monoamine oxidase (MAO) activity was investigated in a series of 60 patients with chronic schizophrenic illnesses free from neuroleptic medication, and 70 normal controls. No significant differences in platelet MAO activity or in substrate preference were detected between patients and controls, using tryptamine and tyramine as substrates. Platelet MAO activity did not distinguish patients with positive symptoms from those with negative symptoms alone and did not show any relationship with severity of disease or with a number of clinical features. These findings suggest that low platelet MAO activity cannot be regarded as a genetic marker for schizophrenia. Important determinants of platelet MAO activity yet to be discovered may have contributed to the discrepancies in recent observations of platelet MAO activity in schizophrenia.
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A case is reported in which platelet monoamine oxidase (MAO) activity fluctuated in the course of a schizophreniform psychosis in a way which suggests a direct relationship between low levels of MAO activity and the psychosis.
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A neurochemical evaluation of the dopamine hypothesis of schizophrenia has been carried out. There was no evidence to suggest that the synthesis or inactivation of dopamine was abnormal in schizophrenia. The brain concentrations of the amine itself, its metabolities and the activities of its related enzymes were similar in controls and schizophrenics. However in vitro and in vivo evidence is presented that suggests that the illness may be associated with an increase in the numbers of dopamine D2 receptors in the brain.