Recent advances of small molecule fluorescent probes for distinguishing monoamine oxidase-A and monoamine oxidase-B in vitro and in vivo

2021 ◽  
Vol 55 ◽  
pp. 101686
Author(s):  
Chang'e Jian ◽  
Jiaxu Yan ◽  
Hang Zhang ◽  
Jianwei Zhu
Keyword(s):  
Monoamine Oxidase ◽  
Small Molecule ◽  
Fluorescent Probes ◽  
Monoamine Oxidase A ◽  
Monoamine Oxidase B ◽  
Recent Advances

Selective binding to monoamine oxidase A: In vitro and in vivo evaluation of 18F-labeled β-carboline derivatives

2015 ◽  
Vol 23 (3) ◽  
pp. 612-623 ◽  
Author(s):  
Hanno Schieferstein ◽  
Markus Piel ◽  
Friderike Beyerlein ◽  
Hartmut Lüddens ◽  
Nicole Bausbacher ◽  
...  
Keyword(s):  
Monoamine Oxidase ◽  
Monoamine Oxidase A ◽  
In Vivo Evaluation ◽  
Selective Binding

Brain monoamine oxidase A in hyperammonemia is regulated by NMDA receptors

2009 ◽  
Vol 4 (3) ◽  
pp. 321-326
Author(s):  
Elena Kosenko ◽  
Yury Kaminsky
Keyword(s):  
Oxidative Stress ◽  
Nmda Receptor ◽  
Monoamine Oxidase ◽  
Nmda Receptors ◽  
Monoamine Oxidase A ◽  
Mk 801 ◽  
Mao A ◽  
Vitro Effect

AbstractMitochondrial enzyme monoamine oxidase A (MAO-A) generates hydrogen peroxide (H2O2) and is up-regulated by Ca2+ 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 Ca2+ 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 H2O2 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.

[P3-321]: IN VIVO AND IN VITRO DEMONSTRATION OF [18 F]THK5351 BINDING TO MONOAMINE OXIDASE-B IN THE HUMAN BRAIN

2017 ◽  
Vol 13 (7S_Part_22) ◽  
pp. P1071-P1072
Author(s):  
Kok Pin Ng ◽  
Tharick A. Pascoal ◽  
Min Su Kang ◽  
Sulantha S. Mathotaarachchi ◽  
Joseph Therriault ◽  
...  
Keyword(s):  
Monoamine Oxidase ◽  
Human Brain ◽  
Monoamine Oxidase B

11C-harmine as a tracer for monoamine oxidase a (MAO-A): In vitro and in vivo studies

1997 ◽  
Vol 24 (4) ◽  
pp. 287-293 ◽  
Author(s):  
Mats Bergström ◽  
Göran Westerberg ◽  
Bengt Långström
Keyword(s):  
Monoamine Oxidase ◽  
Monoamine Oxidase A ◽  
In Vivo Studies ◽  
Mao A

Inhibitor structure-guided design and synthesis of near-infrared fluorescent probes for monoamine oxidase A (MAO-A) and its application in living cells and in vivo

2019 ◽  
Vol 55 (17) ◽  
pp. 2477-2480 ◽  
Author(s):  
Zhengmin Yang ◽  
Wenxiu Li ◽  
Hua Chen ◽  
Qingyuan Mo ◽  
Jun Li ◽  
...  
Keyword(s):  
Monoamine Oxidase ◽  
Fluorescent Probes ◽  
Near Infrared ◽  
Living Cells ◽  
Monoamine Oxidase A ◽  
Specific Detection ◽  
Design And Synthesis ◽  
Mao A ◽  
In Cells

A series of near-infrared fluorescent probes based on inhibitor (clorgyline) structure-guided design were synthesized for the specific detection of MAO-A in cells and in vivo.

IN VIVO AND IN VITRO DEMONSTRATION OF [18F]THK5351 BINDING TO MONOAMINE OXIDASE–B IN THE HUMAN BRAIN

2017 ◽  
Vol 13 (7) ◽  
pp. P142-P143
Author(s):  
Kok Pin Ng ◽  
Tharick A. Pascoal ◽  
Min Su Kang ◽  
Sulantha S. Mathotaarachchi ◽  
Joseph Therriault ◽  
...  
Keyword(s):  
Monoamine Oxidase ◽  
Human Brain ◽  
Monoamine Oxidase B

Locomotor Network Maturation Is Transiently Delayed in the MAOA-Deficient Mouse

2000 ◽  
Vol 83 (4) ◽  
pp. 2468-2470 ◽  
Author(s):  
Jean-René Cazalets ◽  
Marie Gardette ◽  
Gérard Hilaire
Keyword(s):  
Monoamine Oxidase ◽  
Swimming Behavior ◽  
Monoamine Oxidase A ◽  
Network Activity ◽  
Deficient Mouse ◽  
In Vitro Experiments ◽  
C3h Mice ◽  
Ventral Roots

In vivo and in vitro experiments were performed in control (C3H) and monoamine oxidase A (MAOA)-deficient (Tg8) neonatal mice to determine whether MAOA deficiency affected spinal locomotor network maturation. Comparing the swimming behaviors at birth in C3H mice with those in Tg8 mice revealed a delayed role for the hindlimbs in Tg8 swimming, even though adult swimming behavior was acquired at postnatal day 14 (P14) in both strains. Analyzing the locomotor network activity in vitro showed that serotonin (5-HT) induced and modulated locomotor-like discharges in hindlimb ventral roots of C3H but not Tg8 neonates. The Tg8 network began, however, to be affected by 5-HT at P11. Thus both in vivo and in vitro results argue for a transient delay of locomotor network maturation in the Tg8 strain.

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