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Open AccessJournal ArticleDOI

Monoamine oxidase: from genes to behavior.

TLDR
MAO A and B knock-out mice are valuable models for investigating the role of monoamines in psychoses and neurodegenerative and stress-related disorders and show increased reactivity to stress.
Abstract
Cloning of MAO (monoamine oxidase) A and B has demonstrated unequivocally that these enzymes are made up of different polypeptides, and our understanding of MAO structure, regulation, and function has been significantly advanced by studies using their cDNA. MAO A and B genes are located on the X-chromosome (Xp11.23) and comprise 15 exons with identical intron-exon organization, which suggests that they are derived from the same ancestral gene. MAO A and B knock-out mice exhibit distinct differences in neurotransmitter metabolism and behavior. MAO A knock-out mice have elevated brain levels of serotonin, norephinephrine, and dopamine and manifest aggressive behavior similar to human males with a deletion of MAO A. In contrast, MAO B knock-out mice do not exhibit aggression and only levels of phenylethylamine are increased. Mice lacking MAO B are resistant to the Parkinsongenic neurotoxin, 1-methyl-4-phenyl-1,2,3,6-tetra-hydropyridine. Both MAO A and B knock-out mice show increased reactivity to stress. These knock-out mice are valuable models for investigating the role of monoamines in psychoses and neurodegenerative and stress-related disorders.

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MAOA-uVNTR genotype predicts interindividual differences in experimental aggressiveness as a function of the degree of provocation

TL;DR: The data indicate the MAOA-uVNTR-genotype to be specifically associated with measures of reactive impulsive experimental aggressiveness in healthy men and women and increases in a fashion linear to the degree of provocation.
Journal ArticleDOI

Monoamine oxidase inhibition during brain development induces pathological aggressive behavior in mice.

TL;DR: Developmental inhibition of MAO activity engenders behavioral effects that parallel those observed in animals with genetic ablation ofMAO function, and provide a possible model for disinhibited aggression, common in clinical populations.
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Synthesis of 3-benzyl-2-substituted quinoxalines as novel monoamine oxidase A inhibitors.

TL;DR: A new series of 3-benzyl-2-substituted quinoxalines synthesized by means of microwave enhancement of nucleophilic substitution reaction involving the corresponding 2-chloroquinoxaline analogs and substituted amines or hydrazine showed more selective inhibitory activity toward MAO-A thanMAO-B.
Journal ArticleDOI

Drugs related to monoamine oxidase activity.

TL;DR: Desirable effects of MAO inhibition include increased availability of monoamine neurotransmitters, decreased oxidative stress, decreased formation of neurotoxins, induction of pro-survival genes and antiapoptotic factors, and improved mitochondrial functions.
Journal ArticleDOI

Parkin Degrades Estrogen Related Receptors to Limit the Expression of Monoamine Oxidases

TL;DR: The results reveal the molecular mechanism by which parkin suppresses the transcription of MAOs to control oxidative stress induced by dopamine oxidation and increase the ubiquitination and degradation of estrogen-related receptors (ERR).
References
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Journal ArticleDOI

Mutation in the α-synuclein gene identified in families with Parkinson's disease

TL;DR: A mutation was identified in the α-synuclein gene, which codes for a presynaptic protein thought to be involved in neuronal plasticity, in the Italian kindred and in three unrelated families of Greek origin with autosomal dominant inheritance for the PD phenotype.
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Some observations upon a new inhibitor of monoamine oxidase in brain tissue.

TL;DR: The hypothesis that in the enzyme prepared, the MAO is a binary system of enzymes each of which has a detectably different sensitivity to this particular inhibitor, is put forward and evidence after dialysis supports this hypothesis.
Journal ArticleDOI

Abnormal behavior associated with a point mutation in the structural gene for monoamine oxidase A

TL;DR: Analytical results indicate that isolated complete MAOA deficiency in this family is associated with a recognizable behavioral phenotype that includes disturbed regulation of impulsive aggression.
Journal ArticleDOI

Aggressive Behavior and Altered Amounts of Brain Serotonin and Norepinephrine in Mice Lacking MAOA

TL;DR: Pup behavioral alterations, including trembling, difficulty in righting, and fearfulness were reversed by the serotonin synthesis inhibitor parachlorophenylalanine, and adults manifested a distinct behavioral syndrome, including enhanced aggression in males.
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