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Ethanol impairment of spontaneous alternation behaviour and associated changes in medial prefrontal glutamatergic gene expression precede putative markers of dependence

Journal article
Authors Christopher Pickering
Johan Alsiö
Julia Morud
Mia Ericson
Trevor W Robbins
Bo Söderpalm
Published in Pharmacology, Biochemistry and Behavior
Volume 132
Pages 63-70
ISSN 0091-3057
Publication year 2015
Published at Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
Pages 63-70
Language en
Links dx.doi.org/10.1016/j.pbb.2015.02.02...
Keywords Alcoholism, Cognitive impairment, GABA, Dopamine, qPCR
Subject categories Biological research on drug dependence

Abstract

Cognitive impairments are observable in over half of cases with alcoholism, deficits in spatial working memory being particularly common. Previously we observed that rats make more alternation errors in a Y-maze test of spontaneous alternation behaviour/spatial working memory after 5-day intermittent ethanol. Here we used qPCR to quantify changes in gene expression accompanying this behavioural impairment. Male Wistar rats were treated with either saline or ethanol (1 or 2.5g/kg) for 5days followed by 2 drug-free days. Brains were dissected after Y-maze analysis and RNA was extracted from the medial prefrontal cortex, hippocampus and nucleus accumbens. Using the Qiagen GABA & Glutamate PCR array we measured changes in these two neurotransmitter systems. A dose of 1g/kg ethanol did not affect spontaneous alternation behaviour or any other behavioural variable. 2.5g/kg significantly decreased % correct alternations (p=0.028) without affecting total distance (p=0.54) and increased time in the choice area (p=0.023) at the Y-maze centre, indicating a possible impairment in decision-making. In the medial prefrontal cortex, 2.5g/kg ethanol decreased mRNA expression of brain-derived neurotrophic factor, NMDA NR2A subunit, mGluR8 receptor, Homer1, the glutamate transporters SLC1a1 and SLC1a6 and Srr. In the nucleus accumbens this dose did not affect mRNA expression of the dopamine D1 or D2 receptors but did upregulate the GABA transporter GAT-3. Even if only correlational, these data suggest that gene expression changes in the medial prefrontal cortex and associated cognitive impairment occur before adaptation of the dopaminergic system and, presumably, drug dependence.

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