Platelets were examined to enable a simultaneous investigation to be made of indolylamine and electrolyte metabolism in affective disorder. No significant differences were detected in either platelet membrane ATPase or adenyl cyclase specific activity in any of the groups of patients studied, when compared with appropriate controls. A reduced Vmax and y for the 5-hydroxy-tryptamine uptake process into platelets was observed in both unipolar and bipolar depressed groups. The Km for this process was not significantly different in any of the patients from that found in control subjects. Lithium therapy was shown not to influence significantly any of the platelet parameters examined. It is suggested that membrane enzyme changes found in some peripheral cells in patients suffering from affective disorder, i.e. reduced Na+ + K+ - ATPase activity in erythrocytes in depression, is not common to all peripheral cells and may or may not reflect central nervous system changes.
We Have recently reported that chronic electroconvulsive seizures (ECS) lead to a long‐lasting increase (up to 6 weeks) in the activity of monoamine oxidase (MAO) in the brain of rats (Pryor and Otis, 1970). Other investigators have shown increased levels of norepinephrine (NE) and 5‐HT, more rapid clearance of intracisternally‐injected [3H]HNE (Kety, Javoy, Thierry, Julou and Glowinski, 1967), and increased tyrosine hydroxylase activity (Musacchio, Julou, Kety and Glowinski, 1969) at 24 h after a series of two ECS daily for 7 days. Together, these data suggest a sustained activation of the 5‐HT and/or NE systems following chronic ECS. We now report the results of a series of experiments in which some of the potential variables that may be involved in the MAO response were investigated and that indicate some biochemical specificity of the response. In these experiments, succinate dehydrogenase (SDH) activity was also assayed to assess possible nonspecific effects of repeated seizures on mitochondrial metabolism and catechol O‐methyltransferase (COMT) activity was determined to see if this extracellular degradative enzyme for NE was affected in the same way as MAO located intracellularly in the mitochondria.
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