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Evidence-Based Complementary and Alternative Medicine
Volume 2012 (2012), Article ID 818451, 12 pages
Research Article

Inhibition of Activity of GABA Transporter GAT1 by -Opioid Receptor

1Max-Planck-Institute for Biophysics, Max-von-Laue-Straße 3, 60438 Frankfurt, Germany
2Laboratory of Molecular Cell Biology, Institute of Biochemistry and Cell Biology and Max-Planck Guest Laboratory, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 320 Yue Yang Road, Shanghai 200031, China
3Department of Neurobiology and Behavior, Center for the Neurobiology of Learning and Memory, University of California, Irvine, CA 92697, USA
4Shanghai Research Center for Acupuncture and Meridians, 199 Guoshoujing Road, Shanghai 201203, China
5NingXia Key Lab of Cerebrocranial Disease, Ningxia Medical University, 1160 Shengli Street, Ningxia Hui Autonomous Region, Yinchuan 750004, China
6Central Institute of Mental Health, BCCN Heidelberg-Mannheim, J5, 68159 Mannheim, Germany
7Institute for Biophysics, Goethe-University Frankfurt, Max-von-Laue-Straße 1, 60438 Frankfurt, Germany

Received 11 September 2012; Revised 4 November 2012; Accepted 4 November 2012

Academic Editor: Ying Xia

Copyright © 2012 Lu Pu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Analgesia is a well-documented effect of acupuncture. A critical role in pain sensation plays the nervous system, including the GABAergic system and opioid receptor (OR) activation. Here we investigated regulation of GABA transporter GAT1 by OR in rats and in Xenopus oocytes. Synaptosomes of brain from rats chronically exposed to opiates exhibited reduced GABA uptake, indicating that GABA transport might be regulated by opioid receptors. For further investigation we have expressed GAT1 of mouse brain together with mouse OR and OR in Xenopus oocytes. The function of GAT1 was analyzed in terms of Na+-dependent [3H]GABA uptake as well as GAT1-mediated currents. Coexpression of OR led to reduced number of fully functional GAT1 transporters, reduced substrate translocation, and GAT1-mediated current. Activation of OR further reduced the rate of GABA uptake as well as GAT1-mediated current. Coexpression of OR, as well as OR activation, affected neither the number of transporters, nor rate of GABA uptake, nor GAT1-mediated current. Inhibition of GAT1-mediated current by activation of OR was confirmed in whole-cell patch-clamp experiments on rat brain slices of periaqueductal gray. We conclude that inhibition of GAT1 function will strengthen the inhibitory action of the GABAergic system and hence may contribute to acupuncture-induced analgesia.