Mobina Roshanaei Mellat - Department of Animal Biology, Faculty of Natural Sciences, University of Tabriz, Tabriz, Iran.
Homeira Hatami - Department of Animal Biology, Faculty of Natural Sciences, University of Tabriz, Tabriz, Iran

Background and Aim : Methamphetamine dependence (addiction) is a serious problem. Oxidative stress has shown to be a promising lead in explaining, at a cellular level, the harmful effects of MA abuse. Buprenorphine is a semisynthetic opioid derived from thebaine, a naturally occurring alkaloid of the opium poppy, Papaver somniferum Buprenorphine is a partial mu receptor agonist originally developed as analgesic but its potential utility for the management of opioid dependence has been discussed since early the 1970. PGC-1a is a transcriptional co-activator that can be induced by oxidative stress and coordinates the expression of multiple antioxidant programs. The primary aim of this study was therefore to investigate the alteration of PGC-1α gene following methamphetamine addiction in male rats that were under treatment of buprenorphine.Methods : 49 male Wistar rats were randomly assigned into seven experimental groups (n=7): Control, Saline, Methamphetamine (10 mg/kg, i.p. for 5 days), Buprenorphine (6 and 10 mg/kg, i.p.), Methamphetamine + Buprenorphine (6 and 10 mg/kg for 5 days). Brain stem tissue was assayed for the expression of P2X4 receptor gene using RT- PCR.Results : amphetamine administration significantly decreased the level of PGC-1a gene in comparison to control group but it was not significant. The expression of PGC-1a gene did not change after the buprenorphine (6 and 10 mg/kg) administration in comparison to control group.Conclusion : : methamphetamine toxicity influenced mitochondria function by changing the level of PGC-1a gene expression. It seems mitochondria biogenesis gene play a role in methamphetamine toxicity.

Buprenorphine, Amphetamine, P2X4 receptor gene