E
Edson X. Albuquerque
Researcher at University of Maryland, Baltimore
Publications - 268
Citations - 18565
Edson X. Albuquerque is an academic researcher from University of Maryland, Baltimore. The author has contributed to research in topics: Nicotinic agonist & Acetylcholine. The author has an hindex of 69, co-authored 268 publications receiving 17395 citations. Previous affiliations of Edson X. Albuquerque include Federal University of Rio de Janeiro & National Institute on Drug Abuse.
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Journal ArticleDOI
Zanos et al . reply
Panos Zanos,Ruin Moaddel,Patrick J. Morris,Polymnia Georgiou,Jonathan Fischell,Greg I. Elmer,Manickavasagom Alkondon,Peixiong Yuan,Heather J. Pribut,Nagendra Singh,Katina Sourou Sylvestre Dossou,Yuhong Fang,Xi Ping Huang,Cheryl L. Mayo,Edson X. Albuquerque,Scott M. Thompson,Craig J. Thomas,Carlos A. Zarate,Todd D. Gould +18 more
TL;DR: It is demonstrated that (2R,6R)-HNK inhibits synaptic NMDARs and subsequently elicits the same signal transduction pathway previously associated with N MDAR inhibition by ketamine, and that the effects of ( 2R, 6R)- HNK on intracellular signalling are coupled to NMD AR inhibition.
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Induction of intramuscular collateral nerve sprouting by neurally applied colchicine.
TL;DR: Results mean that interruption of axonal transport in L4 fibers stimulates intramuscular sprouting of L5 fibers, consistent with Diamond's hypothesis that nerves possess a propensity for collateral growth which is ordinarily repressed by factors that are dependent on axonal Transport.
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Localization by site-directed mutagenesis of a galantamine binding site on α7 nicotinic acetylcholine receptor extracellular domain.
Jürgen Ludwig,Anja Höffle-Maas,Marek Samochocki,Edgar Luttmann,Edson X. Albuquerque,Gregor Fels,Alfred Maelicke +6 more
TL;DR: The data confirm the earlier results that the galantamine binding site is different from the ACh binding site, and suggest that both sites are in close proximity and hence may influence each other in a synergistic fashion.
Journal Article
Meproadifen reaction with the ionic channel of the acetylcholine receptor: potentiation of agonist-induced desensitization at the frog neuromuscular junction.
TL;DR: The actions of the nicotinic noncompetitive antagonist meproadifen on both the acetylcholine (ACh) receptor-ion channel complex and electrically excitable membrane were examined in frog sciatic-nerve sartorius muscle preparations and appear to interact with the closed ionic channel of the ACh receptor in its resting and activated but nonconducting states.
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The Molecular Basis of Anticholinesterase Actions on Nicotinic and Glutamatergic Synapsesa
TL;DR: The pharmacological characterization of another class of toxins, the histrionicotoxins (HTX), isolated from skin secretions of frogs of the family Dendrobatidae, disclosed an important new class of sites on the nicotinic AChR, responsible for allosteric alterations or noncompetitive blockade of neuromuscular transmission.