Catabolism of intracerebroventricularly injected 5-hydroxytryptamine in mouse: effect of coinjection of tryptamine and several pretreatments

1993 ◽  
Vol 71 (3-4) ◽  
pp. 201-204 ◽  
Author(s):  
B. Duff Sloley ◽  
Shuzo Orikasa ◽  
Alan A. Boulton
Keyword(s):  
Monoamine Oxidase ◽  
Receptor Antagonist ◽  
Mouse Brain ◽  
Monoamine Oxidase Inhibitor ◽  
Oxidase Inhibitor ◽  
Nerve Terminals ◽  
Intracerebroventricular Injection ◽  
Hydroxyindoleacetic Acid

The catabolism of intracerebroventricularly injected 5-hydroxytryptamine in mouse brain was investigated. Pretreatment of animals with the 5-hydroxytryptamine type 1 receptor antagonist metergoline, the 5-hydroxytryptamine type 2 receptor antagonist ketanserin, the 5-hydroxytryptamine reuptake inhibitor fluoxetine, or the selective 5-hydroxytryptamine neurotoxin 5,7-dihydroxytryptamine failed to alter the rate of catabolism of intracerebroventricularly administered 5-hydroxytryptamine. The monoamine oxidase inhibitor tranylcypromine effectively blocked degradation of injected 5-hydroxytryptamine and accumulation of 5-hydroxyindoleacetic acid. Coinjection of tryptamine with 5-hydroxytryptamine reduced the rate of conversion of 5-hydroxytryptamine to 5-hydroxyindoleacetic acid. These results indicate that intracerebroventricularly administered 5-hydroxytryptamine is removed by a monoamine oxidase dependent system. This catabolism is not affected by inhibition of presynaptic uptake, 5-hydroxytryptamine receptor type 1 or type 2 blockade, or destruction of serotonergic nerve terminals. The coadministration of tryptamine may prolong the residence period of 5-hydroxytryptamine through competition for monoamine oxidase.Key words: 5-hydroxytryptamine, tryptamine, monoamine oxidase, intracerebroventricular injection, catabolism.

The effects of imidazole-4-acetic acid on cerebral indole amine metabolism

1982 ◽  
Vol 60 (3) ◽  
pp. 308-312
Author(s):  
V. MacMillan
Keyword(s):  
Acetic Acid ◽  
Steady State ◽  
Monoamine Oxidase ◽  
Cerebral Hemisphere ◽  
Monoamine Oxidase Inhibitor ◽  
Oxidase Inhibitor ◽  
Serotonin Metabolism ◽  
Decarboxylase Inhibitor ◽  
Amine Metabolism ◽  
Hydroxyindoleacetic Acid

The effects of imidazole-4-acetic acid (IMA, 100–400 mg/kg) on indole amine metabolism were studied by measurement of the cerebral hemisphere and brain stem contents of tryptophan, 5-hydroxytryptophan (5-HTP), 5-hydroxytryptamine (5-HT), and 5-hydroxyindoleacetic acid (5-HIAA). The results indicated that IMA does not alter the steady-state contents of brain indole amines. Furthermore, IMA failed to alter the levels of 5-HTP, 5-HT, or 5-HIAA in animals pretreated with 3-hydroxybenzyl hydrazine (a decarboxylase inhibitor), pargyline (a monoamine oxidase inhibitor), or probenecid (a compound which blocks 5-HIAA transport out of brain). These results suggest that altered serotonin metabolism is not a factor in the genesis of the behavioral or electroencephalographic changes produced by IMA.

Possible antidepressant/mania-inducing effects of methionine: a reappraisal of the effects of methionine in chronic psychosis using modern diagnostic criteria

1989 ◽  
Vol 4 (3) ◽  
pp. 175-181
Author(s):  
J.F. Lipinski ◽  
R.C. Alexander
Keyword(s):  
Monoamine Oxidase ◽  
Diagnostic Criteria ◽  
Monoamine Oxidase Inhibitor ◽  
Manic Episode ◽  
Oxidase Inhibitor ◽  
Descriptive Data ◽  
Antidepressant Effects ◽  
Chronic Psychosis

SummaryThe authors have reviewed 13 published studies on methionine administration, usually in combination with a monoamine oxidase inhibitor (MAOI), to chronically psychotic patients, using modern (DSM-III) diagnostic criteria. Four of these studies contained sufficient descriptive data to allow reappraisal of the effects. The results of the review suggest that a proportion of the patients experienced the induction of a manic episode/antidepressant effects rather than the reported worsening of schizophrenia while treated with a methionine-MAOI combination. It is suggested that these observations are consistent with recent findings that S-adenosyl-L-methionine (SAMe) has antidepressant and mania-inducing effects.

ROLE OF AN ENDOGENOUS MONOAMINE OXIDASE INHIBITOR, ISATIN, IN SHRSP BRAIN

1995 ◽  
Vol 22 (s1) ◽  
pp. S86-S87 ◽  
Author(s):  
N. Hamaue ◽  
T. Endo ◽  
M. Hirafuji ◽  
N. Yamazaki ◽  
H. Togashi ◽  
...  
Keyword(s):  
Monoamine Oxidase ◽  
Monoamine Oxidase Inhibitor ◽  
Oxidase Inhibitor

scholarly journals Glycaemic control by monoamine oxidase inhibition in a patient with type 1 diabetes

2016 ◽  
Vol 14 (2) ◽  
pp. 163-165 ◽  
Author(s):  
Hamlin Emory ◽  
Neptune Mizrahi
Keyword(s):  
Type 1 Diabetes ◽  
Glycaemic Control ◽  
Monoamine Oxidase ◽  
Monoamine Oxidase Inhibitor ◽  
Combined Treatment ◽  
Insulin Regimen ◽  
Imaging Data ◽  
Monoamine Oxidase Inhibition ◽  
Oxidase Inhibition

We present clinical, electroencephalographic and low-resolution electromagnetic tomography data that support combined treatment with insulin and a monoamine oxidase inhibitor in a patient with type 1 diabetes. We suggest that brain imaging data can identify a subgroup of patients who are likely to benefit from an insulin regimen and monoamine oxidase inhibition to improve glycaemic control, cardiovascular function, normalize the circadian rhythm and restore perception of glycaemic awareness.

Monoamine oxidase inhibitor usage in Hawaii

2010 ◽  
Vol 3 (4) ◽  
pp. 213-215
Author(s):  
Junji Takeshita ◽  
Deborah Goebert ◽  
John Huh ◽  
Brett Lu ◽  
Diane Thompson ◽  
...  
Keyword(s):  
Monoamine Oxidase ◽  
Monoamine Oxidase Inhibitor ◽  
Oxidase Inhibitor
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