Journal ArticleDOI
The glycine-prodrug, milacemide, increases the seizure threshold due to hyperbaric oxygen; prevention by 1-deprenyl
TLDR
The novel glycine-prodrug anticonvulsant milacemide significantly increased (greater than 400% the seizure threshold induced by hyperbaric oxygen) and that this reaction is mediated primarily by monoamine oxidase B is suggested.About:
This article is published in European Journal of Pharmacology.The article was published on 1988-06-10. It has received 24 citations till now. The article focuses on the topics: Milacemide & Seizure threshold.read more
Citations
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Book ChapterDOI
Cyclopropane Derivatives and their Diverse Biological Activities
TL;DR: Natural and synthetic cyclopropanes bearing simple functionalities are endowed with a large spectrum of biological properties ranging from enzyme inhibitions to insecticidal, antifungal, herbicidal, antimicrobial, antibiotic, antibacterial, antitumor and antiviral activities.
Journal ArticleDOI
C) Means to enhance penetration
TL;DR: It is concluded that the prodrug technology alone or in combination with appropriate formulation techniques may offer a promising means to improve the delivery characteristics of several peptide drugs.
Journal ArticleDOI
Effects of zonisamide on dopaminergic system
Motohiro Okada,Sunao Kaneko,Takayuki Hirano,Kazuhisa Mizuno,T. Kondo,Koichi Otani,Yutaka Fukushima +6 more
TL;DR: It is suggested that therapeutic ZNS doses increase DOPA accumulation as well as both intracellular and extracellular DA, DOPA and HVA levels, and that acute and chronic supratherapeutic ZNS dose administrations inhibit DA turnover.
Journal ArticleDOI
New directions in monoamine oxidase A and B selective inhibitors and substrates.
TL;DR: These recent developments have provided new therapeutic perspectives for the management of Parkinson's disease and seizure disorders via the use of selective inhibitors and amino acid amine prodrug substrates of MAO-B.
Journal ArticleDOI
A review of the in vitro and in vivo neurochemical characterization of the NMDA/PCP/Glycine/Ion channel receptor macrocomplex
Paul L. Wood,Tadimeti S. Rao,S. Iyengar,Thomas H. Lanthorn,Joseph B. Monahan,Alex Cordi,Eric T. Sun,Vazquez Michael L,Nancy M. Gray,Patricia C. Contreras +9 more
TL;DR: It is essential to understand that the first generation products in this area may not be optimal pharmacotherapies, such that haracterization of possible receptor subtypes and understanding the molecular biology of the component proteins of the receptor complex will be crucial in the design of the optimal pharmacological modulators of the NMDA receptor complex.
References
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Journal ArticleDOI
Glycine potentiates the NMDA response in cultured mouse brain neurons
J. W. Johnson,P Ascher +1 more
TL;DR: G glycine may facilitate excitatory transmission in the brain through an allosteric activation of the NMDA receptor, and can be observed in outside-out patches as an increase in the frequency of opening of the channels activated by NMDA agonists.
Journal ArticleDOI
Excitotoxity and the NMDA receptor
Steven M. Rothman,John W. Olney +1 more
TL;DR: Evidence is accumulating that the brain damage associated with anoxia, stroke, hypoglycemia, epilepsy, and perhaps neurodegenerative illnesses such as Huntington's disease may be at least partially produced by excessive activation of NMDA receptors.
Journal ArticleDOI
Glycine modulates [3H]MK-801 binding to the NMDA receptor in rat brain.
Journal ArticleDOI
T-DNA integration and expression in a monocot crop plant after induction of Agrobacterium
TL;DR: Transformation of the monocotyledonous crop plant Dioscorea bulbifera (yam) with agrobacteria preincubated by wound substances from dicotylingonous plants, leading to crown gall tumour formation is reported, and direct evidence for the integration of T-DNA into the nuclear genome of this monocotsized crop is presented.
Journal ArticleDOI
Formation of the Neurotransmitter Glycine From the Anticonvulsant Milacemide Is Mediated By Brain Monoamine Oxidase-b
TL;DR: The present data demonstrate that milacemide is a substrate for brain MAO‐B, and its conversion to glycinamide, further transformed to the inhibitory neurotransmitter, glycine, mediated by this enzyme may contribute to its pharmacological activities.