Monoamine oxidase: from genes to behavior.
Jean C. Shih,K. Chen,M. J. Ridd +2 more
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.read more
Citations
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Mitochondrial function and myocardial aging. A critical analysis of the role of permeability transition
Fabio Di Lisa,Paolo Bernardi +1 more
TL;DR: This work analyzes the possible mechanisms through which PTP opening might contribute to age-related myocardial alterations and the available evidence of an increased probability of PTPOpening in mitochondria isolated from aged tissues and examines the current methodological limitations that complicate the elucidation of causal relationships between PTPopening, mitochondrial dysfunction, and myocardials aging.
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A spontaneous point mutation produces monoamine oxidase A/B knock-out mice with greatly elevated monoamines and anxiety-like behavior.
TL;DR: Observed chase/escape and anxiety-like behavior in theMAO A/B KO mice, different from MAO A or B singleKO mice, suggest that varying monoamine levels result in both a unique biochemical and behavioral phenotype.
Journal ArticleDOI
Pro-apoptotic gene expression mediated by the p38 mitogen-activated protein kinase signal transduction pathway.
TL;DR: Data indicate that monoamine oxidase (MAO) may be a target of pro-apoptotic signal transduction by the p38 mitogen-activated protein (MAP) kinase pathway.
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Human monoamine oxidase enzyme inhibition by coffee and beta-carbolines norharman and harman isolated from coffee.
Tomás Herraiz,Carolina Chaparro +1 more
TL;DR: In this paper, "ready to drink" coffee brews exhibited inhibitory properties on recombinant human MAO A and B isozymes catalyzing the oxidative deamination of kynuramine, suggesting that coffee contains compounds acting as MAO inhibitors.
Journal ArticleDOI
Resilience and Developmental Psychopathology
TL;DR: Some of the challenges to resilience research are highlighted and the example of maltreatment is used to illustrate some of these issues.
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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
Olivier Cases,Isabelle Seif,Joseph Grimsby,Patricia Gaspar,Kevin Chen,Sandrine Pournin,Ulrike Müller,Michel Aguet,Charles Babinet,Jean C. Shih,Edward De Maeyer +10 more
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.