Biogenic amines, neuropeptides and substance abuse. Grand Forks, ND, October 17, 1987. Proceedings.
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The effects of serotonin antagonist peritol, cholinolytic atropine, H2-receptor blocker cimetidine and dopaminergic receptor blocker metoclopramide on stress- and exogenous serotonin-induced gastric ulcerogenesis in rats were studied. Peritol was shown to inhibit significantly serotonin- an stress-induced hemorrhagic effect. Similar but less pronounced inhibit produced by metoclopramide and cimetidine. Atropine decreased gastric hemorrhages induced by serotonin but failed to affect stress-induced hemorrhagic lesions. All antagonists tested decreased stress-induced erosions. Erosive lesions stimulated by exogenous serotonin were significantly decreased by atropine only. Metoclopramide known for its cholinomimetic action increased serotonin-induced erosions. It was concluded that serotonin plays an essential role in the pathogenesis of gastric lesions, and its effects suggest the involvement of acetylcholine, histamine and dopamine.
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The effects of histidine and histamine on branchial vascular haemodynamics were studied using the isolated, perfused gill of the tropical cichlid, Oreochromis (Sarotherodon) niloticus. Histidine had no vasoactive effect while histamine induced vasodilatation. Histamine-induced vasodilatation was irreversibly inhibited by the H1 and H2 receptor antagonists, piriton and cimetidine, respectively. This suggests a possible involvement of the non-neurogenic histaminergic system, acting directly via H1 and H2 histamine receptors, in the regulation of branchial vascular haemodynamics in teleosts.
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The studies on the activity of monoamine oxidase from human placenta, using 2-phenylethylamine as a substrate, corroborate the hypothesis on the possible superoxide radical generation upon FAD oxidation at the second (aerobic) stage of monoamine oxidase reaction. It has been shown that hydrogen peroxide, but not other activated O2 forms, was the end product of this reaction. No superoxide radical generation took place in such systems. And therefore, the induction of lipid peroxidation in the presence of catalase was impossible in mitochondrial membranes containing monoamine oxidase and amines oxidized by it.
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Triiodothyronine injections are shown to lower DOPA decarboxylation and 5-hydroxytryptophan decarboxylation activity and also to decrease the intensity of serotonin and norepinephrine oxidative deamination in the rats' brain synaptosomes. Hypothyroidism produced by 6-methylthiouracil administration was accompanied by intensification of the DOPA-decarboxylase activity and monamine oxidase transformation into serotonin and norepinephrine with no parallel occurring essential changes in the 5-hydroxytryptophan decarboxylation.
The mast cell population is heterogeneous concerning its amine precursor and amine uptake. The immature cells incorporate amine precursors, but in more advanced stages of their maturation they take up only 5-HTP. The mature cells do not take up precursors only 5-HT. The thyroid gland and heart muscle mast cells take up the highest amount of 5-HT; this may be related with some specific function of the mast cells in these two organs. Neither of the mast cells would take up histamine, the compound is synthetised by the cells.
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The influence of acetylcholine, norepinephrine and serotonin on the biopotentials of the cortical and subcortical-stem formations of the brain was studied in cats during a chronic experiment with monopolar electrodes. The accumulation of acetylcholine, norepinephrine and serotonin determines the formation of various profiles representing spectral characteristics of the brain electrograms, which, apparently, is conditioned by a temporal specificity of the action produced by the neuromediators on the post-synaptic membranes.
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In Wistar rats, intracisternal administration of 6-hydroxydopamine caused a 3.0-3.5-fold decrease in noradrenaline and dopamine levels whereas 5,7-dihydroxytryptamine led to a 2.5-fold reduction of the serotonin content in the hypothalamus. The degeneration of serotoninergic neurons produced by 5,7-dihydroxytryptamine did not affect passive avoidance response while the lesion of catecholaminergic neurons with 6-hydroxydopamine disturbed it. Participation of the brain monoaminergic system in the mechanisms of conditioning is discussed.
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