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Sensitization to nicotine significantly decreases expression of GABA transporter GAT-1 in the medial prefrontal cortex.

Journal article
Authors Christopher Pickering
Veronica Bergenheim
Helgi B Schiöth
Mia Ericson
Published in Progress in neuro-psychopharmacology & biological psychiatry
Volume 32
Issue 6
Pages 1521-6
ISSN 0278-5846
Publication year 2008
Published at Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
Pages 1521-6
Language en
Links dx.doi.org/10.1016/j.pnpbp.2008.05....
Keywords Animals, DNA Primers, DNA, Complementary, biosynthesis, genetics, Data Interpretation, Statistical, GABA Plasma Membrane Transport Proteins, biosynthesis, drug effects, Hexamethonium Compounds, pharmacology, Male, Motor Activity, drug effects, Neurotransmitter Agents, metabolism, Nicotine, pharmacology, Nicotinic Agonists, pharmacology, Prefrontal Cortex, drug effects, metabolism, RNA, biosynthesis, genetics, Rats, Rats, Wistar, Receptors, GABA-A, biosynthesis, Reverse Transcriptase Polymerase Chain Reaction
Subject categories Pharmacology, Psychiatry

Abstract

This study investigated GABA signaling following induction of behavioural sensitization to nicotine. Rats were repeatedly injected with saline, nicotine or hexamethonium for 18 days and gene expression was measured with qPCR. Nicotine upregulated GABAA alpha1 subunit expression in the nucleus accumbens (p<0.05) while no changes were observed for GABAA alpha3, alpha4 or alpha5. In the medial prefrontal cortex, no change in expression of the GABAA subunits was observed. We found that nicotine significantly decreased expression of the transporter GAT-1/SLC6A1 (p<0.05) in the medial prefrontal cortex while the expression of the GAT-3/SLC6A11 (p<0.05) transporter was increased in the nucleus accumbens. This provides the first evidence of neuroadaptive changes in the GABA system after nicotine sensitization and the first demonstration of an effect on GAT-1 or GAT-3 transporters in the addiction field. The GAT-1 findings also provide evidence for an alternative theory of why most schizophrenic individuals also use tobacco products.

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