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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 promotes prostate cancer cell perineural invasion through SEMA3C/PlexinA2/NRP1–cMET signaling

TL;DR: In this paper, the authors report that monoamine oxidase A (MAOA) is a clinically and functionally important mediator of prostate invasion in PC cells in vitro and tumor innervation in an orthotopic xenograft model.
Journal ArticleDOI

Monoamine oxidase-A Knockdown in Human Neuroblastoma Cells Reveals Protection Against Mitochondrial Toxins

TL;DR: Examining how the mitochondrial enzyme monoamine oxidase‐A influences death and survival mechanisms in human neuroblastoma cells revealed protection against mitochondrial toxins, and endogenous MAO‐A levels influence mitochondrial function, notably complex I activity.
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Selective blockade of serotonin 5-HT2A receptor increases coronary blood flow via augmented cardiac nitric oxide release through 5-HT1B receptor in hypoperfused canine hearts

TL;DR: Immunohistochemical analysis showed that sarpogrelate induced serotonin production in ischemic cardiac myocytes and suggested that the increase in cardiac release of serotonin may increase NO production in the isChemic heart.
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.
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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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