Inhibition of monoamine oxidase by two substrate-analogues, with different preferences for 5-hydroxytryptamine neurons

  title={Inhibition of monoamine oxidase by two substrate-analogues, with different preferences for 5-hydroxytryptamine neurons},
  author={S. K. Kim and Yoshie Toyoshima and Yuichiro Arai and Hiroyasu Kinemuchi and Takeshi Tadano and Katsuyuki Oyama and N. Satoh and Kensuke Kisara},
E(cid:128)ect of (cid:103) -mangostin through the inhibition of 5-hydroxy-tryptamine 2A receptors in 5-fluoro- (cid:97) -methyltryptamine-induced head-twitch responses of mice
The results suggest that (cid:103) mangostin inhibits 5-FMT-induced head-twitch response in mice by blocking 5-HT 2A receptors not by blocking the release of 5- HT from the central neurone.
Multiscale simulation of monoamine oxidase catalyzed decomposition of phenylethylamine analogs
Why p-OMe- and p-Cl-β-Methylphenethylamines Display Distinct Activities upon MAO-B Binding
Density Functional Theory quantum chemical calculations reveal that β-methylation and para-substitution underpin the observed activities sustained by calculated transition state energy barriers, attained conformations and key differences in their interactions in the substrate binding site.
Effect of γ‐mangostin through the inhibition of 5‐hydroxytryptamine2A receptors in 5‐fluoro‐α‐methyltryptamine‐induced head‐twitch responses of mice
The results suggest that γ‐mangostin inhibits 5‐FMT‐induced head‐twitch response in mice by blocking 5‐HT2A receptors not by blocking the release of 5‐ HT from the central neurone.
The Pivotal Neuroinflammatory, Therapeutic and Neuroprotective Role of Alpha-Mangostin
The pivotal role of α- MG in neuroinflammatory disorders is reviewed and it is confirmed that α-MG partakes in the major stages of tumor growth: initiation, promotion, and progression.
Why pOMe-and pCl-beta-Methylphenethylamines Display Distinct Activities uponMAO-B Binding
Despite their structural and chemical commonalities, p-chloro-β-methylphenethylamine and p-methoxy-β-methylphenethylamine display distinct inhibitory and substrate activities upon MAO-B binding.
Revisiting Forbidden Drugs: Chemical and Pharmacological Perspectives Over Psychedelic Indoleamines and Entactogens as Promising Therapeutic Agents
Depression and anxiety disorders are a major challenge for modern psychiatry, especially when shown to be resistant to conventional means of treatment. Over the past decade, psychedelic and


Potentiation of para-hydroxyamphetamine-induced head-twitch response by inhibition of monoamine oxidase type A in the brain.
The present results indicate that p-OHA might induce the HTR by interaction with intraneuronally increased 5-HT, which probably results in5-HT release onto the postsynaptic 5- HT2 receptors.
Studies of monoamine oxidase and semicarbazide-sensitive amine oxidase. II. Inhibition by alpha-methylated substrate-analogue monoamines, alpha-methyltryptamine, alpha-methylbenzylamine and two enantiomers of alpha-methylbenzylamine.
The present results indicate that SSAO can recognize optical isomers and that some alpha-methylated monoamines tested in the present study inhibit S SAO with properties different from those as MAO inhibitors.
Studies on 5-fluoro-alpha-methyltryptamine and p-chloro-beta-methylphenethylamine: determination of the MAO-A or MAO-B selective inhibition in vitro.
Based on the present findings of highly MAO-A- or -B-selective inhibition, these two compounds might prove to be of value in in vivo studies.
5-Hydroxytryptamine release in vivo from a cytoplasmic pool: studies on the 5-HT behavioural syndrome in reserpinized rats.
Results indicate that PCA releases 5-HT into the synapse from a small cytoplasmic pool which is resistant to reserpine and suggest that this newly synthesized compartment of 5- HT represents the 'functional' transmitter pool.
A new selective inhibitor for uptake of serotonin into synaptosomes of rat brain: 3-(p-trifluoromethylphenoxy). N-methyl-3-phenylpropylamine.
Lilly 110140 is a potent and selective inhibitor for uptake of 5-HT into synaptosomes of rat brain and its primary amine derivative did not block the in vivo uptake of NE into rat heart.