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Nathan L. Absalom
Researcher at University of Sydney
Publications - 40
Citations - 1169
Nathan L. Absalom is an academic researcher from University of Sydney. The author has contributed to research in topics: Receptor & GABAA receptor. The author has an hindex of 17, co-authored 38 publications receiving 958 citations. Previous affiliations of Nathan L. Absalom include Garvan Institute of Medical Research & University of New South Wales.
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Journal ArticleDOI
Alpha9 nicotinic acetylcholine receptors and the treatment of pain.
TL;DR: Pharmacological analysis indicates that RgIA and Vc1.1 are selective antagonists of alpha9alpha10 nAChRs, a subset of peptides used offensively by carnivorous marine snails known as Conus that appear to accelerate the recovery of function after nerve injury.
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Coadministered cannabidiol and clobazam: Preclinical evidence for both pharmacodynamic and pharmacokinetic interactions.
Lyndsey L. Anderson,Nathan L. Absalom,Sarah V. Abelev,Ivan K. Low,Peter T. Doohan,Lewis J. Martin,Mary Chebib,Iain S. McGregor,Jonathon C. Arnold +8 more
TL;DR: The present study aimed to address the nature of the interaction between CBD and clobazam to address speculation that the anticonvulsant efficacy of CBD may simply reflect CBD augmenting clobzam exposure.
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α4βδ GABA(A) receptors are high-affinity targets for γ-hydroxybutyric acid (GHB).
Nathan L. Absalom,Laura F. Eghorn,Inge S. Villumsen,Nasiara Karim,Tina Bay,Jesper V. Olsen,Gitte M. Knudsen,Hans Bräuner-Osborne,Bente Frølund,Rasmus P. Clausen,Mary Chebib,Petrine Wellendorph +11 more
TL;DR: The authors' data link specific GHB forebrain binding sites with α4-containing GABAA receptors and postulate a role for extrasynaptic α4δ-containing GHB receptors in GHB pharmacology and physiology to aid in elucidating the molecular mechanisms behind the proposed function of GHB as a neurotransmitter and its unique therapeutic effects in narcolepsy and alcoholism.
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Role of charged residues in coupling ligand binding and channel activation in the extracellular domain of the glycine receptor.
TL;DR: Results indicate that loops 2 and 7 in the extracellular domain play an important role in the mechanism of activation of the glycine receptor although not by a direct electrostatic mechanism.
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Oxytocin prevents ethanol actions at δ subunit-containing GABAA receptors and attenuates ethanol-induced motor impairment in rats.
Michael T. Bowen,Sebastian Peters,Nathan L. Absalom,Mary Chebib,Inga D. Neumann,Iain S. McGregor +5 more
TL;DR: This study provides the first evidence of oxytocin having a direct, non-OTR–mediated effect on GABA–ethanol interactions, and shows a previously unidentified mechanism through which some of these effects may occur.