Conflicting reports on the association between platelet MAO activity and schizophrenia prompted a critical review and determinations on identical samples at one laboratory in Sweden and one in the USA. Samples originated from eight schizophrenics and 27 relatives belonging to a large pedigree, thus ensuring biological homogeneity.In the USA laboratory, a significantly lower MAO activity was found in the schizophrenics when benzylamine or β–phenylethylamine was used as substrate (but not with trypt–amine), while a similar result was obtained in the Swedish laboratory when tryptamine was used (but not with benzylamine or (β–phenylethylamine). Comparisons between materials examined in different laboratories do not seem meaningful until differences in methodologies have been clarified. At present there is neither proof nor disproof of MAO being a “genetic marker” for vulnerability to the schizophrenic disorder.
The effect of repeated treatment of rats for 21 days with the monoamine reuptake inhibitors imipramine, zimeldine, alaproclate (in each case 10 μmol/kg b.i.d.) and the reversible monoamine oxidase‐A inhibitor amiflamine (3 μmol/kg b.i.d.) on brain noradrenergic mechanisms measured at different times of the day and night was investigated. Imipramine treatment produced a down‐regulation of the Bmax for 3H‐dihydroalprenolol binding to cortical β‐adrenoceptors that was not dependent upon the time of day the animals were killed. Zimeldine, on the other hand, reduced both Bmax, and Kd of binding for day‐time, but not night‐time samples. Alaproclate and amiflamine were without effect on the binding. Twenty‐four hour mean values for 1 nM 3H‐p‐aminoclonidine binding to α2‐adrenoceptors were lower for the zimeldine‐treated rats than for the saline‐treated rats. Pineal melatonin concentrations, which are regulated by β‐adrenoceptors, showed a pronounced diurnal rhythm, with the highest concentrations being found at 02:00. At this time point, a lower pineal melatonin content was found after amiflamine treatment, whereas imipramine, zimeldine and alaproclate were without significant effect. The importance of the use of more than one time point and the use of more than one biochemical test for the determination of the effects of repeated antidepressant treatment on central noradrenergic systems measured ex vivo is discussed.
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