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Ethanol effects on electrophysiological properties of astrocytes in striatal brain slices.

Journal article
Authors Louise Adermark
David M Lovinger
Published in Neuropharmacology
Volume 51
Issue 7-8
Pages 1099-108
ISSN 0028-3908
Publication year 2006
Published at Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
Pages 1099-108
Language en
Links dx.doi.org/10.1016/j.neuropharm.200...
Keywords 1-Octanol, pharmacology, Animals, Astrocytes, drug effects, Calcium, physiology, Carbenoxolone, pharmacology, Cell Communication, drug effects, Cell Membrane Permeability, drug effects, Cesium, pharmacology, Chelating Agents, pharmacology, Chlorides, pharmacology, Corpus Striatum, cytology, Egtazic Acid, analogs & derivatives, pharmacology, Ethanol, antagonists & inhibitors, pharmacology, Fluorescent Dyes, analysis, Gap Junctions, drug effects, physiology, Ion Transport, drug effects, Isoquinolines, analysis, Membrane Potentials, drug effects, Microscopy, Fluorescence, Patch-Clamp Techniques, Potassium, physiology, Potassium Channels, drug effects, Potassium Chloride, pharmacology, Rats, Rats, Sprague-Dawley
Subject categories Physiology, Neurobiology, Substance Abuse

Abstract

Ethanol (EtOH) is known to alter neuronal physiology, but much less is known about the actions of this drug on glial function. To this end, we examined acute effects of ethanol on resting and voltage-activated membrane currents in striatal astrocytes using rat brain slices. Ten minutes exposure to 50mM EtOH reduced slope conductance by 20%, increased input resistance by 25% and decreased capacitance by 38% but did not affect resting membrane potential. Current generated by a hyperpolarizing pulse was inhibited in a concentration dependent manner in passive astrocytes, while no significant EtOH effect was observed in complex astrocytes or neurons. The EtOH effect was blocked when intracellular KCl was replaced with CsCl, but not during chelation of intracellular calcium with BAPTA. During blockage of gap junction coupling with high intracellular CaCl(2) or extracellular carbenoxolone the EtOH effect persisted but was reduced. Interestingly, EtOH effects were largely irreversible when gap junctions were open, but were fully reversible when gap junctions were closed. Ethanol also reduced the spread to other cells of Lucifer Yellow dye from individual glia filled via the patch pipette. These data suggest that EtOH inhibits a calcium-insensitive potassium channel, most likely a passive potassium channel, but also affects gap junction coupling in a way that is sustained after ethanol withdrawal. Astrocytes play a critical role in brain potassium homeostasis, and therefore EtOH effects on astrocytic function could influence neuronal activity.

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