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Alterations in ethanol-induced accumbal transmission after acute and long-term zinc depletion

Journal article
Authors Julia Morud
Louise Adermark
Mia Ericson
Bo Söderpalm
Published in Addiction Biology
Volume 20
Issue 1
Pages 170-181
ISSN 1355-6215
Publication year 2015
Published at Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
Pages 170-181
Language en
Links dx.doi.org/10.1111/adb.12096
Keywords Electrophysiology, ethanol consumption, GABA, GlyR, microdialysis, RAT NUCLEUS-ACCUMBENS, GLYCINE RECEPTOR FUNCTION, DOPAMINE RELEASE, REWARD SYSTEM, MODULATION, SENSITIVITY, DEFICIENCY, SUBUNIT, ALCOHOL, TAURINE, Biochemistry & Molecular Biology, Substance Abuse
Subject categories Clinical Medicine

Abstract

Alcoholism is subject to extensive research, but the role of changes in metabolism caused by alcohol consumption has been poorly investigated. Zinc (Zn2+) deficiency is a common metabolic aberration among alcoholics and Zn2+ influences the function of ligand-gated ion channels, known pharmacological targets of ethanol (EtOH). Here, we investigate whether manipulation of extracellular levels of Zn2+ modulates EtOH-induced increases of dopamine (DA) output, as measured by in vivo microdialysis in the rat, and whether voluntary EtOH consumption is altered by Zn2+ deficiency. Our findings show that the Zn2+-chelating agent tricine slowly raises DA levels when perfused in the nucleus accumbens (nAc), whereas the more potent Zn2+ chelator TPEN reduces DA levels. We also show that pre-treatment with either tricine or TPEN blocks the EtOH-induced DA elevation. Chronic Zn2+ deficiency induced by a Zn2+-free diet did not affect EtOH consumption, but excitatory transmission, assessed by striatal field-potential recordings in the nAc shell, was significantly modulated both by Zn2+-free diet and by EtOH consumption, as compared with the EtOH naive controls. The present study indicates that Zn2+ influences EtOH's interaction with the brain reward system, possibly by interfering with glycine receptor and GABA(A) receptor function. This also implies that Zn2+ deficiency among alcoholics may be important to correct in order to normalize important aspects of brain function.

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