TY  - JOUR
A1  - Pu, Lu
A1  - Xu, Nanjie
A1  - Xia, Peng
A1  - Gu, Quanbao
A1  - Ren, Shuanglai
A1  - Fucke, Thomas
A1  - Pei, Gang
A1  - Schwarz, Wolfgang
T1  - Inhibition of activity of GABA transporter GAT1 by δ-opioid receptor
T2  - Evidence-based complementary and alternative medicine : eCAM
N2  - 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 δOR 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 δOR and μOR in Xenopus oocytes. The function of GAT1 was analyzed in terms of Na(+)-dependent [(3)H]GABA uptake as well as GAT1-mediated currents. Coexpression of δOR led to reduced number of fully functional GAT1 transporters, reduced substrate translocation, and GAT1-mediated current. Activation of δOR further reduced the rate of GABA uptake as well as GAT1-mediated current. Coexpression of μOR, as well as μOR activation, affected neither the number of transporters, nor rate of GABA uptake, nor GAT1-mediated current. Inhibition of GAT1-mediated current by activation of δOR 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.
Y1  - 2012
UR  - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/28958
UR  - https://nbn-resolving.org/urn:nbn:de:hebis:30:3-289589
SN  - 1741-4288
SN  - 1741-427X
N1  - Copyright © 2012 Lu Pu et al. This is an open access article distributed under the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0/ , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
VL  - 2012
IS  - Article ID 818451
PB  - Hindawi
CY  - New York, NY
ER  -