The post-ischemic effects on cerebral cortex and basal ganglia monoamine levels and monoamine oxidase (MAO A and B) and catechol-O-methyl transferase (COMT) activities were evaluated in Mongolian gerbils (Meriones unguiculatus) subjected to bilateral common carotid arteries of occlusion for 15 min and reflow for 7 days. Disorders of monoamine metabolism was found in ischemic brain which persisted during the long-term post-ischemia. A rebound increase of norepinephrine and serotonin appeared in early stages (up to 1 h) of post-ischemia both in cerebral cortex and basal ganglia; a rebound increase of dopamine as found only in cerebral cortex. Thereafter, the serotonin level ws enhanced over the control level during the whole post-ischemic period whereas the levels of catecholamines were reduced particularly in basal ganglia. With respect to monoamine content and activities of monoamine degraded enzymes an oscillatory behavior was observed in the post-ischemia. Disorder of the monoamine metabolism found during post-ischemic period possibly contributes to neurological dysfunction after an ischemic insult.
Our results provide support for the psychosomatic concept of Graves' disease. Personality features, temperament traits, and platelet MAO activity of hyperthyroid individuals are different from those in normal controls and correspond to those observed in anxiety disorders. We propose that the observed behavioral and biochemical similaritites between hyperthyroid and anxiety disorder patients represent an equicausality phenomenon, where the same underlying heritable factors, such as variable central monoaminergic activity coupled with temperament-related susceptibility to stress, facilitate phenotypic manifestation of a number of psychosomatic and psychialric disorders--including Graves disease. The observed correlations between personality traits and MAO activity provide support for the hypothesized functional relationship between the underlying central monoaminergic activity and temperament traits associated with anxiety, depression, and impulsivity.
Cerebral ischemia induced by bilateral common carotid artery occlusion (15 min) with and without release (1 hr) served as a model for comparative regional studies of synaptosomal 3H-5-hydroxytryptamine (3H-5-HT) uptake and release in adult and young gerbils. A decreased uptake and an increased release of 5-HT was observed in the adult after ischemia alone and/or ischemia with reflow. At the same time, 5-HT uptake was not affected except in the cortex and the release was reduced in the young. These findings indicate that the same ischemic insults affect differently the synaptosomal uptake and/or release of 5-HT in adult and young brain.
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