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Special Issue Article

Impact of A118G Polymorphism on the Mu Opioid Receptor Function in Pain

Eduardo J López Soto1, Francina Agosti1, Cecilia Catanesi2 and Jesica Raingo1*
1Electrophysiology Laboratories of the Multidisciplinary Institute of Cell Biology (IMBICE), CIC-PBA CONICET, Argentina
2Molecular Genetics Laboratories of the Multidisciplinary Institute of Cell Biology (IMBICE), CIC-PBA CONICET, Argentina
Corresponding Author : Jesica Raingo
Multidisciplinary Institute of Cell Biology (IMBICE)
CIC-PBA CONICET, La Plata, Buenos Aires, Argentina
E-mail: Jraingo@imbice.gov.ar
Received May 21, 2013; Accepted July 04, 2013; Published July 07, 2013
Citation: Soto EJL, Agosti F, Catanesi C, Raingo J (2013) Impact of A118G Polymorphism on the Mu Opioid Receptor Function in Pain. J Pain Relief 2:119. doi: 10.4172/2167-0846.1000119
Copyright: © 2013 Soto EJL, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Mu Opioid Receptor (MOR) activation by exogenous or endogenous agonists causes reduction of pain threshold after a noxious stimulus, relieving pain sensation. MOR is encoded by OPRM1 gene and its messenger RNA suffers extensible modifications by alternative splicing and single nucleotide polymorphisms (SNPs). A118G (N40D) is the most frequent encoding MOR SNP in humans. In this review we discuss the impact of this polymorphism at molecular, cellular and clinical levels. Since some SNPs are unequally distributed among human populations, we also discuss the utility of A118G as an ethnicity marker among worldwide human populations. As an example, we evaluate A118G frequency in an Argentinean human population and compare it with worldwide frequencies extracted from HapMap database.

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