Expression of Functional Human Monoamine Oxidase A and B cDNAs in Mammalian Cells

Lan, Nancy C.; Chen, Chonghong; Shih, Jean C.

doi:10.1111/j.1471-4159.1989.tb09223.x

Cited by 53 publications

(26 citation statements)

References 13 publications

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“…A comparison of the deduced amino acid sequences showed that the A and B forms have subunit molecular weights of 59,700 and 58,000, respectively, and have 70% amino acid sequence identity. Subsequently, we successfully transfected MAO A and B cDNA in mammalian cells and demonstrated that they exhibit substrate and inhibitor specificity similar, respectively, to endogenous MAO A and B (Lan et al 1989a). This work has demonstrated unequivocally that these two isoenzymes are made up of two different polypeptides and are not the same protein differentially modified.…”

Section: Cloning Of Human Liver Mao a And Bmentioning

confidence: 82%

MONOAMINE OXIDASE: From Genes to Behavior

Shih

Chen

Ridd

1999

Annu. Rev. Neurosci.

1,070

764

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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: Cloning Of Human Liver Mao a And Bmentioning

confidence: 82%

MONOAMINE OXIDASE: From Genes to Behavior

Shih

Chen

Ridd

1999

Annu. Rev. Neurosci.

1,070

764

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“…1 JlCi/ml, New England Nuclear, Boston, MA) served as substrate for MAO-B. The assay procedure was a modifIcation of the method described by Pintar et al (1981) and Lan et al (1989). …”

Section: Methodsmentioning

confidence: 99%

MDMA (Ecstasy) Inhibition of MAO Type A and Type B: Comparisons with Fenfluramine and Fluoxetine (Prozac)

Leonardi

Azmitia

1994

Neuropsychopharmacol

143

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“…This eect was also observed with other b-carbolines, namely FG 7142 ( Figure 3G,H) and bCCB ± a putatively endogenous compound ± (data not shown), and on cerebellar granule neurons ( Figure 4E,F). In this latter cell type, LEV also reversed the inhibitory eect of Ro 5-4864, an atypical and controversial negative allosteric modulator of the GABA A receptor related to the benzodiazepine family (Gee et al, 1988;Lan et al, 1989;Puia et al, 1989). The amplitude of GABA currents was 60.7+2.7% of control currents (n=8) at 25 mM of Ro 5-4864, while in the presence of 100 mM LEV, it returned to control levels (96.8+6.6%, n=6).…”

Section: Lev Reverses the Inhibition Of Gaba-gated Currents Induced Bmentioning

confidence: 99%

The anti‐epileptic drug levetiracetam reverses the inhibition by negative allosteric modulators of neuronal GABA‐ and glycine‐gated currents

Rigo

Hans

Nguyen

et al. 2002

British J Pharmacology

302

177

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1 In this study in vitro and in vivo approaches were combined in order to investigate if the antiepileptic mechanism(s) of action of levetiracetam (LEV; Keppra 1 ) may involve modulation of inhibitory neurotransmission. 2 GABA-and glycine-gated currents were studied in vitro using whole-cell patch-clamp techniques applied on cultured cerebellar granule, hippocampal and spinal neurons. Protection against clonic convulsions was assessed in vivo in sound-susceptible mice. The eect of LEV was compared with reference anti-epileptic drugs (AEDs): carbamazepine, phenytoin, valproate, clonazepam, phenobarbital and ethosuximide. 3 LEV contrasted the reference AEDs by an absence of any direct eect on glycine-gated currents. At high concentrations, beyond therapeutic relevance, it induced a small reduction in the peak amplitude and a prolongation of the decay phase of GABA-gated currents. A similar action on GABA-elicited currents was observed with the reference AEDs, except ethosuximide. 4 These minor direct eects contrasted with a potent ability of LEV (EC 50 =1 ± 10 mM) to reverse the inhibitory eects of the negative allosteric modulators zinc and b-carbolines on both GABA A and glycine receptor-mediated responses. . In contrast, the benzodiazepine receptor antagonist¯umazenil (up to 10 mg kg 71) was without any eect on the protection aorded by LEV. 7 The results of the present study suggest that a novel ability to oppose the action of negative modulators on the two main inhibitory ionotropic receptors may be of relevance for the antiepileptic mechanism(s) of action of LEV.

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Expression of Functional Human Monoamine Oxidase A and B cDNAs in Mammalian Cells

Cited by 53 publications

References 13 publications

MONOAMINE OXIDASE: From Genes to Behavior

MONOAMINE OXIDASE: From Genes to Behavior

MDMA (Ecstasy) Inhibition of MAO Type A and Type B: Comparisons with Fenfluramine and Fluoxetine (Prozac)

The anti‐epileptic drug levetiracetam reverses the inhibition by negative allosteric modulators of neuronal GABA‐ and glycine‐gated currents

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