Chronic buprenorphine treatment and PGC-1α gene expression during methamphetamine addiction in male rat

Background and Aim : The prevalence of methamphetamine (MA) use has increased in recent years. The effects of methamphetamine (METH) on pro-oxidant processes and on the production of reactive oxygen species were examined in vivo in the rat brain. Oxidative stress plays a role in MA-induced neurotoxicity. Buprenorphine offers some potential pharmacologic advantages over methadone in the management of opioid addiction. PGC1-α is a master regulator of ROS scavenging enzymes. PGC1-α is also involved in mitochondrial biogenesis that is vital for cell survival. 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 14 days). Brain stem tissue was assayed for the expression of P2X4 receptor gene using RT- PCR.Results : amphetamine administration 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 : Data shows that methamphetamine activate oxidative stress. Changing the level of PGC-1a gene expression indicate the involving of mitochondria in meth toxicity.

کلیدواژه ها:

Buprenorphine ، Amphetamine ، PGC-1a gene