Niloufar abdollahi - Dept. of Animal Sciences, Faculty of Natural Sciences, University of Tabriz, Tabriz, Iran
Homeira Hatami - Dept. of Animal Sciences, Faculty of Natural Sciences, University of Tabriz, Tabriz, Iran
Dariush Shanehbandi - Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
Mohammad Shabani - Institute of Neuropharmacology, Kerman Neuroscience Research Center, Kerman University of Medical Sciences, Kerman, Iran
Reihaneh Sadeghian - Institute of Neuropharmacology, Kerman Neuroscience Research Center, Kerman University of Medical Sciences, Kerman, Iran

Background & Objective: Toll-like receptors (TLRs) are proteins that play key roles in inflammation. METH and buprenorphine (BUP) both modulate pain, but the exact mechanism underlying their antinociceptive effects is unknown. As a result, the expression of TLR۱ and TLR۲ genes was examined in METH rats that had been treated with or without BUP. Materials & Methods: A total of ۷۷ rats were classified into ۱۱ subtypes (n = ۷): control (saline), BUP ۶ or ۱۰ mg/kg, METH (۱۰ mg/kg), METH+BUP ۶ or ۱۰ mg/kg, or withdrawal groups. The treatments were intraperitoneally administered for ۵ or ۱۴ days. RT-PCR evaluated genes expressed in the brain stem area. Results: The results showed that TLR۱ gene expression in the METH group (۱۰ mg/kg; ۵ days) considerably improved compared with the control group. Furthermore, BUP injection (۱۰ mg/kg) acutely decreased TLR۲ gene expression compared with the METH group. In the METH + BUP (۱۰ mg/kg; ۱۴ days) group, TLR۱ expression was higher than in the METH group. The coadministration of METH+BUP (۱۰ mg/kg) acutely decreased TLR۲ gene expression compared with METH. Conclusion: There are limited changes in these genes, and their role in METH consumption and inflammation is unclear. Due to the presence of these two genes in the inflammatory pain and addiction signaling pathways, they may have more clear roles in other parts of the nervous system.

Buprenorphine, Methamphetamine, Brainstem, Toll-like receptors, Inflammation