Differential age-related changes of mao-a and mao-b in mouse brain and pe peripheral organs

Saura, Josep; Richards, J. G.; Mahy, Nicole

doi:10.1016/0197-4580(94)90071-x

Cited by 105 publications

(47 citation statements)

References 60 publications

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“…The distribution of MAO A and B in the brain shows little species variation. MAO A is predominantly found in catecholaminergic neurons, and MAO B is the form most abundant in serotonergic and histaminergic neurons and glial cells (Jahng et al 1997, Luque et al 1995, Saura et al 1994a, Saura et al 1994b, Westlund et al 1988, Willoughby et al 1988. In the brain, the highest concentration of MAO A is found in the locus coerulus, and the highest concentration of MAO B is found in the raphe nuclei (Jahng et al 1997, Saura et al 1994, Willoughby et al 1988.…”

Section: Localization and Development Of Maomentioning

confidence: 99%

MONOAMINE OXIDASE: From Genes to Behavior

Shih

Chen

Ridd

1999

Annu. Rev. Neurosci.

1,089

777

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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.

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Section: Localization and Development Of Maomentioning

confidence: 99%

MONOAMINE OXIDASE: From Genes to Behavior

Shih

Chen

Ridd

1999

Annu. Rev. Neurosci.

1,089

777

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“…High liver MAO-B levels may allow the majority of MPTP introduced i.p. to be converted to MPP+ systematically, preventing it from entering the brain and elicit its effects there (Saura et al, 1993). MPTP sensitivity has in fact been shown to increase with age in mice, perhaps due to the combined effects of age-related reductions in liver MAO-B activity levels along with increased brain levels.…”

Section: Discussionmentioning

confidence: 96%

“…The B isoform of MA0 is found at regionally high levels in the SN and it increases with age in the brain (Fowler et al, 1980;Westlund et al, 1988;Saura et al, 1993). Although MAO-B is expressed primarily in glial and not in dopaminergic cells, hydrogen peroxide has a high membrane permeability and therefore it can induce toxic effects not only within the cell of origin, but also in neighboring cells (Halliwell, 1992).…”

Section: Discussionmentioning

confidence: 99%

Genetic elevation of monoamine oxidase levels in dopaminergic PC12 cells results in increased free radical damage and sensitivity to MPTP

et al. 1996

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Production of hydrogen peroxide as a by‐product of the breakdown of catecholamines by the enzyme monoamine oxidase (MAO) has been hypothesized to contribute to the increased proclivity of dopaminergic neurons for oxidative injury. We established clonal dopaminergic PC12 cell lines which have elevated MAO activity levels resulting from transgenic expression of the B isoform of the enzyme. Both MAO‐A and MAO‐B have relatively equivalent affinities for dopamine, and since PC12 primarily express the A and not the B form of the enzyme, this allowed us to distinguish the transgenic MAO activity in these cells from endogenous using the MAO‐B specific substrate PEA. Elevation of MAO activity levels in the MAO‐B+ cells resulted in higher levels of both free radicals and free radical damage compared with controls. In addition, increased MAO‐B levels within PC12 cells caused a dose‐dependent increase in sensitivity to the toxin MPTP. Our data suggests that oxidation of catecholamines by MAO can contribute to free radical damage in catecholaminergic neurons and that the low MAO‐B activity levels found endogenously in these cells likely accounts for their relative resistance to MPTP toxicity. © 1996 Wiley‐Liss, Inc.

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“…In mammals it has been shown that MAO A and MAO B are encoded by different genes 2,7 and that their expression, as well as being speci®cally regulated in different cell types, also displays age-related changes in both the brain and the peripheral organs. 8 In vitro and in vivo studies have provided substantial evidence that MAO A and MAO B activities are under hormonal control. 9±14 However, studies on the effects of different hormones have often led to con¯icting results, and it is likely that other stimuli, in addition to hormones, are involved in these mechanisms.…”

Section: Introductionmentioning

confidence: 99%

Monoamine oxidase A and B activities in embryonic chick hepatocytes: differential regulation by retinoic acid

Nicotra¹,

Falasca²,

Senatori³

et al. 2001

Cell Biochemistry & Function

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Monoamine oxidases (MAOs) A and B are two isoenzymes involved in the degradation of many biological amines in the nervous system and in peripheral organs. In the present work hepatocytes isolated from 14-day-old chick embryos were used as a model system to determine whether retinoic acid (RA) is capable of modulating the activity of the two MAO forms. RA is a retinoid that, by binding with nuclear receptors, interferes with the expression of specific genes in many differentiation processes. Enzymic activity was measured with a radiochemical method using serotonin and beta-phenylethylamine as preferential substrates for MAO A and MAO B, respectively. The specific activity of the two forms was measured in hepatocytes cultured for 24, 48 and 72 h in the presence and the absence of serum. RA stimulated MAO B but not MAO A activity, in a dose- and time-dependent way, and only in the presence of serum. Maximum stimulation (about 3.5-fold) was obtained after treatment with 5 microM RA for 72 h. Kinetic analysis of MAO B activity showed an increase in V(max) in treated hepatocytes (5 microM RA for 72 h) with no change in K(m). In conclusion, the present work shows that RA selectively elicits MAO B activity in cultured chick embryonic hepatocytes, this stimulation requires the presence of some factors present in the serum and is probably due to an increase in the number of enzyme molecules.

show abstract

Differential age-related changes of mao-a and mao-b in mouse brain and pe peripheral organs

Cited by 105 publications

References 60 publications

MONOAMINE OXIDASE: From Genes to Behavior

MONOAMINE OXIDASE: From Genes to Behavior

Genetic elevation of monoamine oxidase levels in dopaminergic PC12 cells results in increased free radical damage and sensitivity to MPTP

Monoamine oxidase A and B activities in embryonic chick hepatocytes: differential regulation by retinoic acid

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