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
Junctional and extra functional aspects of inherited muscular dystrophy in chickens: development and pharmacology *
TL;DR: A potential therapeutic approach to the dystrophic condition in chickens is presented, along with a discussion of the rationale for such treatment and of the basic membrane defect in muscular dystrophies in chickens.
Journal ArticleDOI
The reversible carbamate, (-)physostigmine, reduces the size of synaptic end plate lesions induced by sarin, an irreversible organophosphate
TL;DR: Pretreatment of rats with atropine and the reversible esterase inhibitor physostigmine [-)PHY, prior to injection of a lethal dose of the irreversible organophosphate sarin, protects 100% of the animals from lethality and shows that damage to the end plate region of voluntary muscles is also strikingly limited by the same pretreatment.
Journal ArticleDOI
The ionic channel of the nicotinic acetylcholine receptor is unable to differentiate between the optical antipodes of perhydrohistrionicotoxin.
TL;DR: Although perhydrohistrionicotoxin contains 4 chiral centers, complete steric inversion does not alter its effects on the acetylcholine receptor—ion channel complex, by contrast the recognition site of the AcChR is extremely sensitive to any change in the chirality of agonists.
Journal ArticleDOI
Interaction of narcotic antagonist naltrexone with nicotinic acetylcholine receptor.
L. Oliveira,B.W. Madsen,N. Kapai,Shebl M. Sherby,K.L. Swanson,Mohyee E. Eldefrawi,Edson X. Albuquerque +6 more
TL;DR: Biphasic functional changes in neuromuscular transmission can be attributed to an allosteric mechanism with increased agonist binding to the nicotinic receptor at nanomolar concentrations and caused a non-competitive blockade of the ionic channel at micromolar concentrations.
Book ChapterDOI
Activation and Inhibition of the Nicotinic Receptor: Actions of Physostigmine, Pyridostigmine and Meproadifen
TL;DR: A large number of studies on biochemical aspects of the nicotinic AChR have been undertaken as well as on primary structural, electronmicroscopic, neutron diffraction, and other analyses (see reviews 3, 4, 18 and 31).