Although the etiology of manic-depressive psychosis is still obscure, its genetic study and the efficacy of somatic treatments such as electroconvulsive shock and psychotropic medication in manic-depressive psychosis would seem to suggest that depression might have a somatic causes). Imipramine type drugs and monoamine oxidase inhibitors (MAOI) affect brain monoamines-catecholamines and 5-hydroxytryptamine (serotonin)-, and the monoamine metabolism has come to be regarded by many workers to have an essential importance in affective disturbances6J8.31). Jensen") and others*) reported that reserpine reduced monoamines in the brain, and that about 15% of hypertensive patients treated with reserpine for long periods of time developed severe depression.Strom-Olsen and weil-Malherbe34) and Shinfuku et al.30) have found higher urinary excretion of norepinephrine in the manic than the retarded depressed phase of the disease. Based on those findings Schildkraut26.27) proposed the catecholamine hypothesis of affective disorders. The hypothesis is as follows: depressions are associated with an absolute or relative decrease in catecholamines, particularly norepinephrine, available at central adrenergic receptor sites.On the other hand Twarog and Page36) and Woolley and Shaw") gave an attention to the role of serotonin in the central nervous system. Brodie et al.5) emphasized that the tranquilizing action of reserpine is associated with variations in brain serotonin level and not in brain norepinephrine level. Coppen et al.7) found that the urinary excretion of tryptamine in depressive patients was about half of normal and that it returned to normal on clinical recovery. Ashcroft et a1.2) and Dencker et al.11) found that the cerebrospinal fluid in depressive patients contained reduced amounts of 5-hydroxyindolacetic acid (SHIAA), a metabolite of serotonin. Stevens et al.33) demonstrated the presence of a positive correlation between mood and urinary excretion of 5HIAA. However, the amount of urinary 5HIAA is markedly influenced by water and alcohol intakelo.2*). On the metabolism of serotonin in vivo, Hosodal6) reported that, in addition to the pathway to SHIAA, there exist several different metabolic pathways of serotonin leading either to serotonin-o-glucuronite, or 5-hydroxytryptophole etc. Therefore, it is more reliable to determine serum serotonin than the urinary excretion of 5HIAA. No report has been published on the serum serotonin level in manic-depressive
The diurnal rhythmicity of glutamic acid decarboxylase (GAD) activity in the nucleus level of the rat brain was examined by the radiochemical micromethod in a light-dark condition. GAD activity showed a biphasic variation in globus pallidus and substantia nigra (zona reticulata and compacta), but a monophasic variation, i.e. high in the dark, in colliculus superior (stratum griseum superficiale and stratum opticum). As for hypothalamus GAD activity of some nuclei (N. arcuatus, N. periventricularis, N. preopticus, etc.) it indicated a monophasic variation, while that of some nuclei (N. suprachiasmaticus, N. ventromedialis, A. lateralis, etc.) it showed no significant variations despite their proved functional activity with rhythmicity.
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