The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)



Gene Review

Maoa  -  monoamine oxidase A

Mus musculus

Synonyms: 1110061B18Rik, AA407771, MAO-A, Monoamine oxidase type A
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.

Disease relevance of Maoa


Psychiatry related information on Maoa


High impact information on Maoa

  • We examined allele-specific expression of the X-linked monoamine oxidase type A (MAOA) gene and the expression of nine additional X-linked genes in nine cloned XX calves [10].
  • 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 [11].
  • 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 [11].
  • We now report that pargyline, nialamide and tranylcypromine, which inhibit both MAO-A and MAO-B, when administered to mice before MPTP, protect against MPTP-induced dopaminergic neurotoxicity [12].
  • Aggressive behavior and altered amounts of brain serotonin and norepinephrine in mice lacking MAOA [13].

Chemical compound and disease context of Maoa


Biological context of Maoa

  • Observed chase/escape and anxiety-like behavior in the MAO A/B KO mice, different from MAO A or B single KO mice, suggest that varying monoamine levels result in both a unique biochemical and behavioral phenotype [1].
  • A spontaneous point mutation produces monoamine oxidase A/B knock-out mice with greatly elevated monoamines and anxiety-like behavior [1].
  • This mutation caused a nonsense-mediated mRNA decay and resulted in the absence of MAO A transcript, protein, and catalytic activity and abrogates a DraI restriction site [1].
  • Autoradiographical distribution of imidazoline binding sites in monoamine oxidase A deficient mice [18].
  • As previously suggested to explain the raphe autoreceptor loss in 2-month-old MAO-A KO mice, the overall 5-HT1AR down-regulation in mutant pups probably results from extracellular 5-HT excess in both raphe and target structures [19].

Anatomical context of Maoa


Associations of Maoa with chemical compounds

  • Brain levels of serotonin, norepinephrine, dopamine, and phenylethylamine increased, and serotonin metabolite 5-hydroxyindoleacetic acid levels decreased, to a much greater degree than in either MAO A or B single KO mice [1].
  • A reduction in binding to the I(2)-BS, as labelled by both [(3)H]idazoxan and [(3)H]2-BFI (2-(2-benzofuranyl)-2-imidazoline), was seen in the MAO-A knockout animals in both brain and kidney sections, whereas binding to the I(1)-BS in kidney sections remained unchanged [18].
  • Data are discussed with reference to the ectopic 5-HT uptake and accumulation reported to occur during the first 10 postnatal days in wild-type and MAO-A KO mice [19].
  • The selectivity of the separate assays is further enhanced by the use of inhibitors, deprenyl to block MAO-B and clorgyline to block MAO-A [21].
  • Deficiency in the monoamine degradation enzyme monoamine oxidase A (MAOA) or prenatal exposure to the monoamine uptake inhibitor cocaine alters behavior in humans and rodents, but the mechanisms are unclear [22].

Regulatory relationships of Maoa


Other interactions of Maoa

  • The binding of [(3)H]Ro19-6327 to MAO-B was unaffected, indicating no change in this isoform in response to the loss of MAO-A [18].
  • 5-HT1AR binding was then analyzed in four MAO-A mutant vs. five wild-type neonatal brains, from olfactory bulb to cervical cord [19].
  • The anx mutation was correlated with decreased MAOA mRNA in the LC (but not RN), decreased 5HTT mRNA in the RN, and a trend towards lower NET mRNA in the LC [25].
  • Elevated levels of aggression have been reported in mice lacking the monoamine oxidase A and the 5-HT1B receptor genes [26].
  • This study suggested that the 5-HT circadian rhythm is regulated by TPH and AANAT but not the MAO A gene in this cell line [27].

Analytical, diagnostic and therapeutic context of Maoa


  1. A spontaneous point mutation produces monoamine oxidase A/B knock-out mice with greatly elevated monoamines and anxiety-like behavior. Chen, K., Holschneider, D.P., Wu, W., Rebrin, I., Shih, J.C. J. Biol. Chem. (2004) [Pubmed]
  2. Role for monoamine oxidase-A (MAO-A) in the bioactivation and nigrostriatal dopaminergic neurotoxicity of the MPTP analog, 2'Me-MPTP. Kindt, M.V., Youngster, S.K., Sonsalla, P.K., Duvoisin, R.C., Heikkila, R.E. Eur. J. Pharmacol. (1988) [Pubmed]
  3. Activities of monoamine oxidase-A and -B are altered in the brains of congenitally hyperammonemic sparse-fur (spf) mice. Rao, V.L., Qureshi, I.A., Butterworth, R.F. Neurosci. Lett. (1994) [Pubmed]
  4. Effects of angiotensin II on brain monoamine oxidase activity in non-hypoxic and hypoxic mice. Stancheva, S., Georgiev, V., Alova, L., Getova, D. Acta physiologica et pharmacologica Bulgarica. (1996) [Pubmed]
  5. Development of fluorinated 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine analogs with potent nigrostriatal toxicity for potential use in positron emission tomography studies. Harik, S.I., Riachi, N.J., Hritz, M.A., Berridge, M.S., Sayre, L.M. J. Pharmacol. Exp. Ther. (1993) [Pubmed]
  6. Lack of barrels in the somatosensory cortex of monoamine oxidase A-deficient mice: role of a serotonin excess during the critical period. Cases, O., Vitalis, T., Seif, I., De Maeyer, E., Sotelo, C., Gaspar, P. Neuron (1996) [Pubmed]
  7. Selective enhancement of emotional, but not motor, learning in monoamine oxidase A-deficient mice. Kim, J.J., Shih, J.C., Chen, K., Chen, L., Bao, S., Maren, S., Anagnostaras, S.G., Fanselow, M.S., De Maeyer, E., Seif, I., Thompson, R.F. Proc. Natl. Acad. Sci. U.S.A. (1997) [Pubmed]
  8. MAO A knockout attenuates adrenocortical response to various kinds of stress. Popova, N.K., Maslova, L.N., Morosova, E.A., Bulygina, V.V., Seif, I. Psychoneuroendocrinology (2006) [Pubmed]
  9. Monoamine oxidase A knockout mice exhibit impaired nicotine preference but normal responses to novel stimuli. Agatsuma, S., Lee, M., Zhu, H., Chen, K., Shih, J.C., Seif, I., Hiroi, N. Hum. Mol. Genet. (2006) [Pubmed]
  10. Aberrant patterns of X chromosome inactivation in bovine clones. Xue, F., Tian, X.C., Du, F., Kubota, C., Taneja, M., Dinnyes, A., Dai, Y., Levine, H., Pereira, L.V., Yang, X. Nat. Genet. (2002) [Pubmed]
  11. Monoamine oxidase: from genes to behavior. Shih, J.C., Chen, K., Ridd, M.J. Annu. Rev. Neurosci. (1999) [Pubmed]
  12. Protection against the dopaminergic neurotoxicity of 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine by monoamine oxidase inhibitors. Heikkila, R.E., Manzino, L., Cabbat, F.S., Duvoisin, R.C. Nature (1984) [Pubmed]
  13. Aggressive behavior and altered amounts of brain serotonin and norepinephrine in mice lacking MAOA. Cases, O., Seif, I., Grimsby, J., Gaspar, P., Chen, K., Pournin, S., Müller, U., Aguet, M., Babinet, C., Shih, J.C. Science (1995) [Pubmed]
  14. Effect of nonselective and selective inhibitors of monoamine oxidases A and B on pethidine toxicity in mice. Boden, R., Botting, R., Coulson, P., Spanswick, G. Br. J. Pharmacol. (1984) [Pubmed]
  15. alpha-Methylated tryptamine derivatives induce a 5-HT receptor-mediated head-twitch response in mice. Tadano, T., Neda, M., Hozumi, M., Yonezawa, A., Arai, Y., Fujita, T., Kinemuchi, H., Kisara, K. Neuropharmacology (1995) [Pubmed]
  16. Inhibition of MAO B, but not MAO A, blocks DSP-4 toxicity on central NE neurons. Gibson, C.J. Eur. J. Pharmacol. (1987) [Pubmed]
  17. MAO inhibitors, clorgyline and lazabemide, prevent hydroxyl radical generation caused by brain ischemia/reperfusion in mice. Suzuki, T., Akaike, N., Ueno, K., Tanaka, Y., Himori, N. Pharmacology (1995) [Pubmed]
  18. Autoradiographical distribution of imidazoline binding sites in monoamine oxidase A deficient mice. Anderson, N.J., Seif, I., Nutt, D.J., Hudson, A.L., Robinson, E.S. J. Neurochem. (2006) [Pubmed]
  19. Reduced density of functional 5-HT1A receptors in the brain, medulla and spinal cord of monoamine oxidase-A knockout mouse neonates. Lanoir, J., Hilaire, G., Seif, I. J. Comp. Neurol. (2006) [Pubmed]
  20. Developmental expression of monoamine oxidases A and B in the central and peripheral nervous systems of the mouse. Vitalis, T., Fouquet, C., Alvarez, C., Seif, I., Price, D., Gaspar, P., Cases, O. J. Comp. Neurol. (2002) [Pubmed]
  21. Rapid and simultaneous determination of monoamine oxidase A and monoamine oxidase B activities in mouse brain homogenates by liquid chromatography with electrochemical detection. Freeman, K.B., Bulawa, M.C., Zeng, Q., Blank, C.L. Anal. Biochem. (1993) [Pubmed]
  22. Excessive activation of serotonin (5-HT) 1B receptors disrupts the formation of sensory maps in monoamine oxidase a and 5-ht transporter knock-out mice. Salichon, N., Gaspar, P., Upton, A.L., Picaud, S., Hanoun, N., Hamon, M., De Maeyer , E., Murphy, D.L., Mossner, R., Lesch, K.P., Hen, R., Seif, I. J. Neurosci. (2001) [Pubmed]
  23. Modulation of tyrosine hydroxylase and aromatic L-amino acid decarboxylase after inhibiting monoamine oxidase-A. Cho, S., Duchemin, A.M., Neff, N.H., Hadjiconstantinou, M. Eur. J. Pharmacol. (1996) [Pubmed]
  24. Enhancement of 5-hydroxytryptamine-induced head-twitch response after olfactory bulbectomy. Nakagawasai, O., Tadano, T., Arai, Y., Hozumi, S., Oba, A., Tan-No, K., Yasuhara, H., Kisara, K., Oreland, L. Neuroscience (2003) [Pubmed]
  25. Differential expression of monoamine oxidase A, serotonin transporter, tyrosine hydroxylase and norepinephrine transporter mRNA by anorexia mutation and food deprivation. Jahng, J.W., Houpt, T.A., Joh, T.H., Son, J.H. Brain Res. Dev. Brain Res. (1998) [Pubmed]
  26. Dissecting the role of the serotonin system in neuropsychiatric disorders using knockout mice. Gingrich, J.A., Hen, R. Psychopharmacology (Berl.) (2001) [Pubmed]
  27. The circadian rhythm of 5-HT biosynthetic and degradative enzymes in immortalized mouse neuroendocrine pineal cell line--a model for studying circadian rhythm. Yeung Lam, P., Chen, K., Shih, J.C. Life Sci. (2004) [Pubmed]
  28. Attenuation of MPTP-induced dopaminergic neurotoxicity by TV3326, a cholinesterase-monoamine oxidase inhibitor. Sagi, Y., Weinstock, M., Youdim, M.B. J. Neurochem. (2003) [Pubmed]
  29. Age-related changes on MAO in Bl/C57 mouse tissues: a quantitative radioautographic study. Saura, J., Richards, J.G., Mahy, N. J. Neural Transm. Suppl. (1994) [Pubmed]
WikiGenes - Universities