Intracellular distribution of monoamine oxidase A in selected regions of rat and monkey brain and spinal cord

Westlund, Karin N.; Krakower, Terri J.; Kwan, Sau-Wah; Abell, Creed W.

doi:10.1016/0006-8993(93)91664-e

Cited by 78 publications

(41 citation statements)

References 19 publications

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“…MAO has been localized in rodent, cat, primate, and human brain by a variety of techniques, including immunohistochemistry (Levitt et al 1982, Westlund 1994, Westlund et al 1985, Westlund et al 1988, Westlund et al 1993, Willoughby et al 1988, enzyme autoradiography (Saura et al 1996, Saura et al 1992, and in situ hybridization (Jahng et al 1997, Saura et al 1996. The distribution of MAO A and B in the brain shows little species variation.…”

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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Section: Gene Expression Is Required For Ngf Withdrawal-induced Apoptmentioning

confidence: 99%

“…Two isoforms of MAO (A and B) are expressed in the brain (35,36). MAO A is found predominantly in the substantia nigra (a region rich in dopaminergic neurons), the locus coeruleus, the striatum, and other areas containing catecholaminergic neurons (36,37). MAO B is expressed at a lower level in the same brain regions as MAO A and is most abundant in the raphe nuclei and glial cells (35,38).…”

Section: Gene Expression Is Required For Ngf Withdrawal-induced Apoptmentioning

confidence: 99%

Pro-apoptotic gene expression mediated by the p38 mitogen-activated protein kinase signal transduction pathway

Zutter

Davis

2001

Proc. Natl. Acad. Sci. U.S.A.

118

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Neurotrophic factor deprivation causes apoptosis by a mechanism that requires macromolecular synthesis. This fact suggests that gene expression is necessary to achieve cell death. To identify mRNA that is expressed in apoptotic cells we used subtractive hybridization with cDNA prepared from neuronal pheochromocytoma cells. Monoamine oxidase (MAO) expression was increased in cells during nerve growth factor withdrawal-induced apoptosis. The increased apoptosis and induction of MAO was prevented by inhibition of the p38 mitogen-activated protein (MAP) kinase pathway. MAO may contribute to the apoptotic process because inhibition of MAO activity suppressed cell death. Together, these data indicate that MAO may be a target of pro-apoptotic signal transduction by the p38 MAP kinase pathway.

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“…The enzyme has important functions in the metabolism of monoamine neurotransmitters in the central nervous system. In the brain, there are two sub-types, MAO-A mainly in neurons [1] and MAO-B in glial cells [2]. MAO-A preferentially oxidizes serotonine, norepinephrine and epinephrine, whereas MAO-B preferentially degrades benzylamine and phenylethylamine.…”

Section: Introductionmentioning

confidence: 99%

Brain monoamine oxidase A in hyperammonemia is regulated by NMDA receptors

Kosenko

Kaminsky

2009

Open Life Sciences

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Mitochondrial enzyme monoamine oxidase A (MAO-A) generates hydrogen peroxide (H 2 O 2 ) and is up-regulated by Ca 2+ and presumably by ammonia. We hypothesized that MAO-A may be under the control of NMDA receptors in hyperammonemia. In this work, the in vivo effects of single dosing with ammonia and NMDA receptor antagonist MK-801 and the in vitro effect of Ca 2+ on MAO-A activity in isolated rat brain mitochondria were studied employing enzymatic procedure. Intraperitoneal injection of rats with ammonia led to an increase in MAO-A activity in mitochondria indicating excessive H 2 O 2 generation. Calcium added to isolated mitochondria stimulated MAO-A activity by as much as 84%. MK-801 prevented the in vivo effect of ammonia, implying that MAO-A activation in hyperammonemia is mediated by NMDA receptors. These data support the conclusion that brain mitochondrial MAO-A is regulated by the function of NMDA receptors. The enzyme can contribute to the oxidative stress associated with hyperammonemic conditions such as encephalopathy and Alzheimer's disease. The attenuation of the oxidative stress highlights MAO-A inactivation and NMDA receptor antagonists as sources of novel avenues in the treatment of mental disorders.

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Intracellular distribution of monoamine oxidase A in selected regions of rat and monkey brain and spinal cord

Cited by 78 publications

References 19 publications

MONOAMINE OXIDASE: From Genes to Behavior

MONOAMINE OXIDASE: From Genes to Behavior

Pro-apoptotic gene expression mediated by the p38 mitogen-activated protein kinase signal transduction pathway

Brain monoamine oxidase A in hyperammonemia is regulated by NMDA receptors

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