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On the Action of General Anesthetics on Cellular Function: Barbiturate Alters the Exocytosis of Catecholamines in a Model Cell System

Journal article
Authors Daixin Ye
Andrew G Ewing
Published in Chemphyschem
Volume 19
Issue 10
Pages 1173-1179
ISSN 1439-4235
Publication year 2018
Published at Department of Chemistry and Molecular Biology
Pages 1173-1179
Language en
Keywords barbiturate, catecholamines, electrochemistry, exocytosis, vesicles, protein-kinase-c, adrenal chromaffin cells, fusion pore kinetics, amperometric measurements, induced unconsciousness, release, vesicles, transmitters, fluorescence, synaptosomes, Chemistry, Physics
Subject categories Physical Sciences, Electrochemistry


General anesthetics are essential in many areas, however, the cellular mechanisms of anesthetic-induced amnesia and unconsciousness are incompletely understood. Exocytosis is the main mechanism of signal transduction and neuronal communication through the release of chemical transmitters from vesicles to the extracellular environment. Here, we use disk electrodes placed on top of PC12 cells to show that treatment with barbiturate induces fewer molecules released during exocytosis and changes the event dynamics perhaps by inducing a less stable fusion pore that is prone to close faster during partial exocytosis. Larger events are essentially abolished. However, use of intracellular vesicle impact electrochemical cytometry using a nano-tip electrode inserted into a cell shows that the distribution of vesicle transmitter content does not change after barbiturate treatment. This indicates that barbiturate selectively alters the pore size of larger events or perhaps differentially between types of vesicles. Alteration of exocytosis in this manner could be linked to the effects of general anesthetics on memory loss.

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