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Biogenic amines administration

Tujimori K, Nabeshima T, Ho IK, et al. 1982b. Effect of oral administration of chlordecone and mirex on brain biogenic amines in mice. Neurotoxicology 3(2) 143-148. [Pg.255]

Kanada M, Miyagawa M, Sato M, et al. 1994. Neurochemical profile of effects of 28 neurotoxic chemicals on the central nervous system in rats (1) effects of oral administration on brain contents of biogenic amines and metabolites, hid Health 32 145-164. [Pg.272]

Serendipity has played a major role in the discovery of most classes of psychotropic drugs. For example, the observation that the first antidepressants, the tricyclic antidepressants and the monoamine oxidase inhibitors, impeded the reuptake of biogenic amines into brain slices, or inhibited their metabolism, following their acute administration to rats, provided the experimenter with a mechanism that could be easily investigated in vitro. Such methods led to the development of numerous antidepressants that differed in their potency, and to some extent in their side effects (for example, the selective serotonin reuptake inhibitors) but did little to further the development of novel antidepressants showing greater therapeutic efficacy. The accidental discovery of atypical antidepressants such as mianserin led to the broadening of the basis of the animal models... [Pg.109]

Depression. Depression is our most common mental problem. One in four women and one in ten men will have a major depression during their lifetime.1095 More than 15 million people in the United States are affected by severe depression in any given year and more than 30,000 may commit suicide.1096 1097 Worldwide psychiatric problems, mostly depression, account for 28% of all disabilities.1098 The biogenic amine hypothesis states that depression results from the depletion of neurotransmitters in the areas of the brain involved in sleep, arousal, appetite, sex drive, and psychomotor activity. An excess of transmitters is proposed to give rise to the manic phase of the bipolar (manic-depressive) cycle that is sometimes observed. In support of this hypothesis is the observation that administration of reserpine precipitates depression, which may be serious in 15-20% of hypertensive patients receiving the drug. Similar effects are observed with the dopa decarboxylase inhibitor a-methyldopa... [Pg.1808]

Flora, S.J.S., Saxena, G., Gautam, P., Kaur, P., Gill, K.D. (2007a). Lead induced oxidative stress and alterations in biogenic amines in different rat brain regions and their response to combined administration of DMSA and MiADMSA. Chem. Biol. Interact. 170 209-20. [Pg.129]

However, these neurochemical effects are acute. That is to say, biogenic amine reuptake is blocked within minutes of drug administration. The therapeutic effects, on the other hand, in ameliorating or reversing the symptoms of major depression, require repeated antidepressant drug administration. Though some improvement in symptoms is often noted during the... [Pg.500]

Eriksson H, Lenngren S, Heilbronn E. 1987a. Effect of long-term administration of manganese on biogenic amine levels in discrete striatal regions of rat brain. Arch Toxicol 59 426-431. [Pg.452]

Komura J, Sakamoto M. 1992b. Effects of manganese forms on biogenic amines in the brain and behavioral alterations in the mouse Eong-term oral administration of several manganese compounds. Environ Res 57 34-44. [Pg.465]

Komura J and Sakamoto M. 1994. Chronic oral administration of methylcyclopentadienyl manganese tricarbonyl altered brain biogenic amines in the mouse comparison with inorganic manganese. Toxicol Eett 73 65-73. [Pg.465]

Effects on other receptors are known (e.g., antimuscarinic and antihistaminic), but these appear to elicit mostly side effects. The hypothesis that arises—and may replace the biogenic amine concept partially—is that it may be the chronic exposure of central (32-adrenoreceptors to these elevated biogenic amines (NE, 5-HT, and maybe DA also) that is the basis of the action. The most likely effect now seems to be decreased sensitivity of these receptors. By measuring c-AMP levels, studies using long-term drug administration indicate that central (3-receptors become less responsive postsynaptically and also that central 5-HT and (Xi receptors may become enhanced. [Pg.614]

Similar caution should be exercised with biogenic amine uptake blockers such as tricyclic antidepressants. Amphetamine is contraindicated in advanced arteriosclerosis symptomatic cardiovascular disease moderate to severe hypertension hyperthyroidism hypersensitivity or idiosyncrasy to the sympathomimetic amines glaucoma agitated states history of drug abuse and during or within 14 days following administration of monoamine oxidase (MAO) inhibitors. [Pg.195]

Oral ingestion of up to 1 mmol (ca. 100 mg) of histamine does not elicit toxic symptoms in normal individuals (Motil and Scrimshaw, 1979). However, vasodilation and increased heart rate result on intravenous administration of 0.07 /imol, demonstrating the importance of histamine-metabolizing enzymes in the digestive tract. More research is needed to define nontoxic levels of histamine in foods which may contain other substances that potentiate the action of histamine, e.g., putrescine and cadaver-ine (Bjeldanes etal., 1978). Construction of an overall biogenic amine index may be valuable for the establishment of regulatory fimits (Joosten, 1988). [Pg.291]

Since morphine releases histamine from central stores [292] and chronic administration of histamine alters brain catecholamine levels [300], it has also been proposed that opiate-induced changes in central concentrations or tissue levels of other biogenic amines may be initiated by decreases in brain histamine [295], Whilst a role for brain histamine has yet to be determined in the antinociceptive effects of the narcotic analgesics, this amine may interact with one or more other amines to subserve the antinociceptive, tolerance and physical dependence effects of morphine-like agents. [Pg.273]

Biogenic amine content in foods is subject to European legislation under Directive 91/439/ EEC, which allows up to a limit of 100 mg/kg of histamine in fishery products. The U.S. Food and Drug Administration (FDA, 2011) has set the limit of histamine tolerance in foods in general at 50 mg/kg. The European Food Safety Authority (EFSA, 2011) has also set a limit for meat products of 50 mg/kg for histamine and up to 600 mg/kg for tyramine. [Pg.677]

Papavasiliou and colleagues demonstrated an intracellular increase in the concentration of manganese in liver tissue after the administrations of DA, L-epinephrine, or DL-isoproterenol. It was also observed that this effect was mediated through an intracellular increase in cyclic 3, 5 -adenosine monophosphate. Although the importance of these studies in relation to manganese encephalopathy could not be evaluated, it became clear that a correlation existed between manganese metabolism and biogenic amines. [Pg.179]


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Biogenics

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