Methamphetamine Provokes Neuronal Atrophy in Prefrontal Cortex

Methamphetamine (METH) is an addictive psychostimulant drug that induces damage on brain reward system. Prefrontal cortex (PFC) is a part of mesocordical pathway which plays an essential role in drug addiction. Recent reports highlighted that METH induces neurotoxicity via several pathways namely neuroinflammation and apoptosis. The present study is performed to examine the alteration of inflammationand apoptosis pathways in PFC under the influence of METH. Materials and Methods: the male rats were intraperitoneal injected with 15 mg METH (5mg in first day and 10mg in second day). The rats were euthanized and decapitated 24h after last injection. RNA was extracted from PFC tissue. Then the relative expression level of TNFα, IL1β and IL10 (as inflammation associated genes), CASP8 (extrinsic apoptosis relatedcandidate) as well as AKT and mROR (regulatory related candidates) were evaluated in comparison with controls. Results: The qPCR results displayed a significant increase in expression of pro-inflammatory cytokine TNFα and IL1β along with remarkably decreases inanti- inflammatory cytokine IL10 in METH treated groups. Moreover, METH augmented the expression level CASP8 considerably. The relative expression of AKT and mTOR were significantly declined upon METH treatment. Conclusion: METH induced neuronal atrophy in PFC via activation of the neuro inflammation and apoptosis pathways.