dc.creatorWang, Dian Shi
dc.creatorPenna, Antonello
dc.creatorOrser, Beverley A.
dc.date.accessioned2019-03-18T11:55:28Z
dc.date.available2019-03-18T11:55:28Z
dc.date.created2019-03-18T11:55:28Z
dc.date.issued2017
dc.identifierAnesthesiology, Volumen 126, Issue 4, 2018, Pages 666-677
dc.identifier15281175
dc.identifier00033022
dc.identifier10.1097/ALN.0000000000001483
dc.identifierhttps://repositorio.uchile.cl/handle/2250/166960
dc.description.abstract© 2016, the American Society of Anesthesiologists, Inc. Wolters Kluwer Health, Inc. All Rights Reserved.Background: The dissociative general anesthetic ketamine is a well-known N-methyl-d-aspartate receptor antagonist. However, whether ketamine, at clinically relevant concentrations, increases the activity of inhibitory γ-aminobutyric acid (GABA) receptor type A (GABAA) receptors in different brain regions remains controversial. Here, the authors studied the effects of ketamine on synaptic and extrasynaptic GABAA receptors in hippocampal neurons. Ketamine modulation of extrasynaptic GABAA receptors in cortical neurons was also examined. Methods: Whole cell currents were recorded from cultured murine neurons. Current evoked by exogenous GABA, miniature inhibitory postsynaptic currents, and currents directly activated by ketamine were studied. Results: Ketamine did not alter the amplitude, frequency, or kinetics of postsynaptic currents but increased a tonic inhibitory current generated
dc.languageen
dc.publisherLippincott Williams and Wilkins
dc.rightshttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/
dc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile
dc.sourceAnesthesiology
dc.subjectAnesthesiology and Pain Medicine
dc.titleKetamine Increases the Function of γ-Aminobutyric Acid Type A Receptors in Hippocampal and Cortical Neurons
dc.typeArtículo de revista


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