Ontogenesis of Multiple Forms of Monoamine Oxidase in Rat Brain Regions and Liver

Tsang, D.; Ho, Kwok-Ping; Wen, Huajie

doi:10.1159/000112258

Cited by 18 publications

(6 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…MAO A is almost at adult levels at birth whereas MAO B activity increases several-fold with aging (Diez & Maderdrut 1977, Lewinsohn et al 1980, Saura et al 1994, Tsang et al 1986. Because MAO B is predominantly located in glial cells (Levitt et al 1982, Westlund et al 1985, the large increase in MAO B with aging may be attributable to the proliferation of these cells.…”

Section: Localization and Development Of Maomentioning

confidence: 99%

MONOAMINE OXIDASE: From Genes to Behavior

Shih

Chen

Ridd

1999

Annu. Rev. Neurosci.

1,099

777

View full text Add to dashboard Cite

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 knockout 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 knockout 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-tetrahydropyridine. Both MAO A and B knock-out mice show increased reactivity to stress. These knockout mice are valuable models for investigating the role of monoamines in psychoses and neurodegenerative and stress-related disorders.

show abstract

Section: Localization and Development Of Maomentioning

confidence: 99%

MONOAMINE OXIDASE: From Genes to Behavior

Shih

Chen

Ridd

1999

Annu. Rev. Neurosci.

1,099

777

View full text Add to dashboard Cite

show abstract

“…MAOA-deficient mice exhibit enhanced startle behavior and decreased exploration of novel environments (Cases et al, 1995;Chen et al, 2004). These behavioral phenotypes correlate with increased monoamine levels specifically in postnatal life, as the gradual rise in monoamine oxidase B (MAOB) normalizes adult monoamine metabolism (Tsang et al, 1986). Whereas MAOA activity impacts 5-HT, DA, and NE levels, 5-HTT function selectively regulates 5-HT signaling.…”

Section: -Ht and Emotional And Cognitive Behaviormentioning

confidence: 99%

Monoamine-Sensitive Developmental Periods Impacting Adult Emotional and Cognitive Behaviors

Suri

Teixeira

Cagliostro

et al. 2014

Neuropsychopharmacol

145

125

View full text Add to dashboard Cite

Development passes through sensitive periods, during which plasticity allows for genetic and environmental factors to exert indelible influence on the maturation of the organism. In the context of central nervous system development, such sensitive periods shape the formation of neurocircuits that mediate, regulate, and control behavior. This general mechanism allows for development to be guided by both the genetic blueprint as well as the environmental context. While allowing for adaptation, such sensitive periods are also vulnerability windows during which external and internal factors can confer risk to disorders by derailing otherwise resilient developmental programs. Here we review developmental periods that are sensitive to monoamine signaling and impact adult behaviors of relevance to psychiatry. Specifically, we review (1) a serotonin-sensitive period that impacts sensory system development, (2) a serotonin-sensitive period that impacts cognition, anxiety-and depressionrelated behaviors, and (3) a dopamine-and serotonin-sensitive period affecting aggression, impulsivity and behavioral response to psychostimulants. We discuss preclinical data to provide mechanistic insight, as well as epidemiological and clinical data to point out translational relevance. The field of translational developmental neuroscience has progressed exponentially providing solid conceptual advances and unprecedented mechanistic insight. With such knowledge at hand and important methodological innovation ongoing, the field is poised for breakthroughs elucidating the developmental origins of neuropsychiatric disorders, and thus understanding pathophysiology. Such knowledge of sensitive periods that determine the developmental trajectory of complex behaviors is a necessary step towards improving prevention and treatment approaches for neuropsychiatric disorders.

show abstract

“…(3) The increases of 5-HT and NE in MAO A KO mice compared to normal mice are age-dependent in the postnatal period. Differences are likely influenced by the natural developmental delay in the maturation of MAO B enzymatic activity seen in the neonate and young adult [38,78], as well as by the increasing importance of adaptational mechanisms which compensate for the underlying absence of MAO A activity. Such mechanisms could include decreases in substrate synthesis and/or enhancement of alternate metabolic routes.…”

Section: Phenotype Of Mao A-deficient Mice Biochemical Changesmentioning

confidence: 99%

Biochemical, behavioral, physiologic, and neurodevelopmental changes in mice deficient in monoamine oxidase A or B

Holschneider

Chen²,

Seif

et al. 2001

Brain Research Bulletin

View full text Add to dashboard Cite

The availability of mutant mice that lack either MAO A or MAO B has created unique profiles in the central and peripheral availability of serotonin, norepinephrine, dopamine, and phenylethylamine. This paper summarizes some of the current known phenotypic findings in MAO A knock-out mice and contrast these with those of MAO B knock-out mice. Differences are discussed in relation to the biochemical, behavioral, and physiologic changes investigated to date, as well as the role played by redundancy mechanisms, adaptational responses, and alterations in neurodevelopment.

show abstract

Ontogenesis of Multiple Forms of Monoamine Oxidase in Rat Brain Regions and Liver

Cited by 18 publications

References 13 publications

MONOAMINE OXIDASE: From Genes to Behavior

MONOAMINE OXIDASE: From Genes to Behavior

Monoamine-Sensitive Developmental Periods Impacting Adult Emotional and Cognitive Behaviors

Biochemical, behavioral, physiologic, and neurodevelopmental changes in mice deficient in monoamine oxidase A or B

Contact Info

Product

Resources

About