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.

The effects of the anticonvulsant valproic acid on cerebral indole amine metabolism

1979 ◽  
Vol 57 (8) ◽  
pp. 843-847 ◽  
Author(s):  
V. MacMillan
Keyword(s):  
Valproic Acid ◽  
Cerebral Hemisphere ◽  
Transport Mechanism ◽  
Monoamine Oxidase Inhibitor ◽  
Oxidase Inhibitor ◽  
Decarboxylase Inhibitor ◽  
Amine Metabolism ◽  
Hydroxyindoleacetic Acid ◽  
The Brain ◽  
Tryptophan Hydroxylation

The effects of valproic acid (500 mg/kg, ip, 1 h prior to testing) on indole amine metabolism were studied in rats by measurement of the contents of tryptophan, 5-hydroxytryptophan (5-HTP), 5-hydroxytryptamine (5-HT), and 5-hydroxyindoleacetic acid (5-HIAA) in the cerebral hemisphere. Tryptophan and 5-HIAA levels were increased, whereas 5-HTP and 5-HT remained unchanged. Furthermore, valproic acid failed to alter the levels of 5-HTP and DOPA, 5-HT and DA, and 5-HIAA in animals pretreated, respectively, with 3-hydroxybenzyl hydrazine (a decarboxylase inhibitor), pargyline (a monoamine oxidase inhibitor), or probenecid (a compound which blocks 5-HIAA transport out of the brain and cerebrospinal fluid). These results militate against the possibility that valproic acid alters the rate of tryptophan hydroxylation or the synthesis of 5-HT. However they do support the concept that valproic acid increases brain 5-HIAA by inhibition of the transport mechanism which removes 5-HIAA from the brain.

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 acute hypercapnia on cerebral indole amine metabolism

1978 ◽  
Vol 56 (2) ◽  
pp. 223-226 ◽  
Author(s):  
V. MacMillan
Keyword(s):  
Monoamine Oxidase ◽  
Cerebral Hemisphere ◽  
Tryptophan Hydroxylase ◽  
Monoamine Oxidase Inhibition ◽  
Decarboxylase Inhibition ◽  
Amine Metabolism ◽  
Hydroxyindoleacetic Acid ◽  
Oxidase Inhibition ◽  
Increased Activity ◽  
Synthesis And Degradation

The effects of 1-h exposure to hypercapnia ([Formula: see text], 90–110 mmHg) on cerebral indole amine metabolism were studied in rats by measurement of cerebral hemisphere contents of tryptophan, 5-hydroxytryptophan (5-HTP), 5-hydroxytryptamine (5-HT), and 5-hydroxyindoleacetic acid (5-HIAA). 5-HIAA content was increased after 1-h exposure to hypercapnia, whereas tryptophan, 5-HTP, and 5-HT remained unchanged from control. The accumulation of 5-HTP after decarboxylase inhibition with 3-hydroxybenzyl hydrazine was increased in hypercapnic rats and indicated an increased activity of tryptophan hydroxylase. During the 1-h exposure to hypercapnia there was increased accumulation of 5-HT after monoamine oxidase inhibition with pargyline and increased accumulation of 5-HIAA arter probenecid. The results indicate an increased synthesis and degradation of indole amines in acute hypercapnia.

Effects of chronic monoamine oxidase inhibitor treatment on biogenic amine metabolism in rat brain

1979 ◽  
Vol 18 (10) ◽  
pp. 771-776 ◽  
Author(s):  
D.S. Robinson ◽  
I.C. Campbell ◽  
Margaret Walker ◽  
Nancy J. Statham ◽  
W. Lovenberg ◽  
...  
Keyword(s):  
Monoamine Oxidase ◽  
Rat Brain ◽  
Biogenic Amine ◽  
Monoamine Oxidase Inhibitor ◽  
Oxidase Inhibitor ◽  
Amine Metabolism ◽  
Inhibitor Treatment

Amine Metabolism after an Overdose of a Monoamine Oxidase Inhibitor

1962 ◽  
Vol 267 (9) ◽  
pp. 421-426 ◽  
Author(s):  
Eugene T. Baldridge ◽  
Leona V. Miller ◽  
Bernard J. Haverback ◽  
Shannon Brunjes
Keyword(s):  
Monoamine Oxidase ◽  
Monoamine Oxidase Inhibitor ◽  
Oxidase Inhibitor ◽  
Amine Metabolism

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

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

Identification of Kaempferol as a Monoamine Oxidase Inhibitor and Potential Neuroprotectant in Extracts ofGinkgo BilobaLeaves

2000 ◽  
Vol 52 (4) ◽  
pp. 451-459 ◽  
Author(s):  
B. D. SLOLEY ◽  
L. J. URICHUK ◽  
P. MORLEY ◽  
J. DURKIN ◽  
J. J. SHAN ◽  
...  
Keyword(s):  
Monoamine Oxidase ◽  
Monoamine Oxidase Inhibitor ◽  
Oxidase Inhibitor
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