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Kosenko, Elena; Венедиктова, Н. И.; Kaminsky, Yury G.

doi:10.1023/a:1025834232678

Cited by 8 publications

(1 citation statement)

References 20 publications

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“…In neurons, ion fluxes during the action potential result in transient changes in the calcium ion concentration in the cytosol, but uptake by the endoplasmic reticulum and mitochondria quickly restore the normal low micromolar level. Calcium (Ca 2+ ) was found to increase MAO activity in mitochondria and cells [127][128][129][130]. When a short burst of Ca 2+ was induced in mice by a calcium channel agonist, the increase in MAO A activity was transient [130].…”

Section: Biological Questions 71 Does Variation In the Calcium Ion Concentration Change Mao Activity?mentioning

confidence: 99%

Questions in the Chemical Enzymology of MAO

Ramsay

Albreht

2021

Chemistry

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We have structure, a wealth of kinetic data, thousands of chemical ligands and clinical information for the effects of a range of drugs on monoamine oxidase activity in vivo. We have comparative information from various species and mutations on kinetics and effects of inhibition. Nevertheless, there are what seem like simple questions still to be answered. This article presents a brief summary of existing experimental evidence the background and poses questions that remain intriguing for chemists and biochemists researching the chemical enzymology of and drug design for monoamine oxidases (FAD-containing EC 4.1.3.4).

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Section: Biological Questions 71 Does Variation In the Calcium Ion Concentration Change Mao Activity?mentioning

confidence: 99%

Questions in the Chemical Enzymology of MAO

Ramsay

Albreht

2021

Chemistry

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Alzheimer disease-related presenilin-1 variants exert distinct effects on monoamine oxidase-A activity in vitro

et al. 2011

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Monoamine oxidase-A (MAO-A) has been associated with both depression and Alzheimer disease (AD). Recently, carriers of AD-related presenilin-1 (PS-1) alleles have been found to be at higher risk for developing clinical depression. We chose to examine whether PS-1 could influence MAO-A function in vitro. Overexpression of selected AD-related PS-1 variants (wildtype, Y115H, ΔEx9 and M146V) in mouse hippocampal HT-22 cells affects MAO-A catalytic activity in a variant-specific manner. The ability of the PS-1 substrate-competitor DAPT to induce MAO-A activity in cells expressing either PS-1 wildtype or PS-1(M146V) suggests the potential for a direct influence of PS-1 on MAO-A function. In support of this, we were able to co-immunoprecipitate MAO-A with FLAG-tagged PS-1 wildtype and M146V proteins. This potential for a direct protein-protein interaction between PS-1 and MAO-A is not specific for HT-22 cells as we were also able to co-immunoprecipitate MAO-A with FLAG-PS-1 variants in N2a mouse neuroblastoma cells and in HEK293 human embryonic kidney cells. Finally, we demonstrate that the two PS-1 variants reported to be associated with an increased incidence of clinical depression [e.g., A431E and L235V] both induce MAO-A activity in HT-22 cells. A direct influence of PS-1 variants on MAO-A function could provide an explanation for the changes in monoaminergic tone observed in several neurodegenerative processes including AD. The ability to induce MAO-A catalytic activity with a PS-1/γ-secretase inhibitor should also be considered when designing secretase inhibitor-based therapeutics.

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Distinct effects of ketamine and acetyl l-carnitine on the dopamine system in zebrafish

Robinson

Dumas

Cuevas

et al. 2016

Neurotoxicology and Teratology

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Ketamine, a noncompetitive N-methyl-d-aspartic acid (NMDA) receptor antagonist is commonly used as a pediatric anesthetic. We have previously shown that acetyl L-carnitine (ALCAR) prevents ketamine toxicity in zebrafish embryos. In mammals, ketamine is known to modulate the dopaminergic system. NMDA receptor antagonists are considered as promising anti-depressants, but the exact mechanism of their function is unclear. Here, we measured the levels of dopamine (DA) and its metabolites, 3, 4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), in the zebrafish embryos exposed to ketamine in the presence and absence of 0.5 mM ALCAR. Ketamine, at lower doses (0.1–0.3 mM), did not produce significant changes in DA, DOPAC or HVA levels in 52 h post-fertilization embryos treated for 24 h. In these embryos, tyrosine hydroxylase (TH) mRNA expression remained unchanged. However, 2 mM ketamine (internal embryo exposure levels equivalent to human anesthetic plasma concentration) significantly reduced DA level and TH mRNA indicating that DA synthesis was adversely affected. In the presence or absence of 2 mM ketamine, ALCAR showed similar effects on DA level and TH mRNA, but increased DOPAC level compared to control. ALCAR reversed 2 mM ketamine-induced reduction in HVA levels. With ALCAR alone, the expression of genes encoding the DA metabolizing enzymes, MAO (monoamine oxidase) and catechol-O-methyltransferase (COMT), was not affected. However, ketamine altered MAO mRNA expression, except at the 0.1 mM dose. COMT transcripts were reduced in the 2 mM ketamine-treated group. These distinct effects of ketamine and ALCAR on the DA system may shed some light on the mechanism on how ketamine can work as an anti-depressant, especially at sub-anesthetic doses that do not affect DA metabolism and suppress MAO gene expression.

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Untitled

Cited by 8 publications

References 20 publications

Questions in the Chemical Enzymology of MAO

Questions in the Chemical Enzymology of MAO

Alzheimer disease-related presenilin-1 variants exert distinct effects on monoamine oxidase-A activity in vitro

Distinct effects of ketamine and acetyl l-carnitine on the dopamine system in zebrafish

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