In vivo evidence for the reversible action of the monoamine oxidase inhibitor brofaromine on 5-hydroxytryptamine release in rat brain

1995 ◽  
Vol 351 (5) ◽  
Author(s):  
Nuria Bel ◽  
Francesc Artigas
Keyword(s):  
Monoamine Oxidase ◽  
Rat Brain ◽  
Monoamine Oxidase Inhibitor ◽  
Oxidase Inhibitor

Biosynthesis of Cerebral Phenolic Amines. I. In Vivo Formation of p-Tyramine, Octopamine, and Synephrine

1972 ◽  
Vol 50 (3) ◽  
pp. 261-267 ◽  
Author(s):  
Alan A. Boulton ◽  
P. H. Wu
Keyword(s):  
Monoamine Oxidase ◽  
Monoamine Oxidase Inhibitor ◽  
Oxidase Inhibitor ◽  
Intraventricular Injection

Following the intraventricular injection of 14C-labelled dopamine, p-tyrosine, and p-tyramine to rats pretreated with a monoamine oxidase inhibitor, the labelled phenolic amines p-tyramine, octopamine, and synephrine were isolated and identified as their DNS derivatives. Differences in the amounts of the phenolicamines formed suggest that mechanisms other than just decarboxylation are involved.

Stress causes an increase in endogenous monoamine oxidase inhibitor (tribulin) in rat brain

1988 ◽  
Vol 92 (2) ◽  
pp. 218-221 ◽  
Author(s):  
S.K. Bhattacharya ◽  
Vivette Glover ◽  
I. McIntyre ◽  
G. Oxenkrug ◽  
M. Sandler
Keyword(s):  
Monoamine Oxidase ◽  
Rat Brain ◽  
Monoamine Oxidase Inhibitor ◽  
Oxidase Inhibitor

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

scholarly journals 4-Aminobutyrate in mammalian putrescine catabolism

1975 ◽  
Vol 152 (2) ◽  
pp. 201-210 ◽  
Author(s):  
N. Seiler ◽  
B. Eichentopf
Keyword(s):  
Monoamine Oxidase ◽  
Diamine Oxidase ◽  
Monoamine Oxidase Inhibitor ◽  
Mitochondrial Pathway ◽  
Oxidase Inhibitor ◽  
Catabolic Pathway ◽  
Oxidative Deamination ◽  
Aminobutyrate Aminotransferase ◽  
Derivatives Of

The effects of inhibitors of diamine oxidase (EC 1.4.3.6), monoamine oxidase (EC 1.4.3.4) and 4-aminobutyrate aminotransferase (EC 2.6.1.19) on the catabolism of putrescine in mice in vivo were studied. Diamine oxidase inhibitors and carboxymethoxylamine (amino-oxyacetate) markedly inhibit the metabolism of [14C]putrescine to 14CO2, but affect different enzymes. Aminoguanidine specifically inhibits the mitochondrial and non-mitochondrial diamine oxidases, whereas carboxymethoxylamine specifically inhibits 4-aminobutyrate transamination by the mitochondrial pathway. Hydrazine inhibits at both sites, and results in increased concentrations of 4-aminobutyrate in brain and liver. Pretreatment of mice with carboxymethoxylamine and [14C]putrescine leads to the urinary excretion of amino[14C]butyrate. Carboxymethoxylamine does not affect the non-mitochondrial pathway of putrescine catabolism, as the product of oxidative deamination of putrescine in the extramitochondrial compartment is not further oxidized but is excreted in the urine as derivatives of 4-aminobutyraldehyde. Another catabolic pathway of putrescine involves monoamine oxidase, and the monoamine oxidase inhibitor, pargyline, decreases the metabolism of [14C]putrescine to 14CO2in vivo. Catabolism of putrescine to CO2in vivo occurs along different pathways, both of which have 4-aminobutyrate as a common intermediate, in contrast with the non-mitochondrial catabolism of putrescine, which terminates in the excretion of 4-aminobutyraldehyde derivatives. The significance of the different pathways is discussed.

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