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Disentangling the Role of Astrocytes in Alcohol Use Disorder

Journal article
Authors Louise Adermark
M. S. Bowers
Published in Alcoholism-Clinical and Experimental Research
Volume 40
Issue 9
ISSN 0145-6008
Publication year 2016
Published at Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
Language en
Links dx.doi.org/10.1111/acer.13168
Keywords Astrocyte, Gliotransmission, Glutamate, Alcohol Use Disorder, glutamate transporter glast, sensitive eaat2 expression, gap-junction, permeability, ventral tegmental area, rat nucleus-accumbens, preferring, p rats, nf-kappa-b, primary cultures, in-vivo, ethanol-consumption, Substance Abuse
Subject categories Neuroscience

Abstract

Several laboratories recently identified that astrocytes are critical regulators of addiction machinery. It is now known that astrocyte pathology is a common feature of ethanol (EtOH) exposure in both humans and animal models, as even brief EtOH exposure is sufficient to elicit long-lasting perturbations in astrocyte gene expression, activity, and proliferation. Astrocytes were also recently shown to modulate the motivational properties of EtOH and other strongly reinforcing stimuli. Given the role of astrocytes in regulating glutamate homeostasis, a crucial component of alcohol use disorder (AUD), astrocytes might be an important target for the development of next-generation alcoholism treatments. This review will outline some of the more prominent features displayed by astrocytes, how these properties are influenced by acute and long-term EtOH exposure, and future directions that may help to disentangle astrocytic from neuronal functions in the etiology of AUD.

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