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Showing 2 results for Methamphetamine
Reza Shahbazi, Homiera Hatami Nemati, Hatam Ahmadi, Faezehe Zogoulipour,
Volume 9, Issue 2 (3-2022)
Abstract
Introduction: Methamphetamine is a nerve stimulant. Buprenorphine has been widely used in the management of various types of pain and reducing addiction side effects. This study aimed to investigate the role of methamphetamine, buprenorphine, or their interaction on analgesic threshold and the expression of protein kinase B (AKT) and glycogen synthase kinase 3 (GSK3b) genes in the lumbar spinal cord of male rats.
Materials and Methods: In this experimental study, 56 male Wistar rats (weight 200 ± 50 g) were randomly divided into eight groups: The control group, sham group, methamphetamine group, two buprenorphine groups, two methamphetamines + buprenorphine groups, and deprivation group. The drugs of methamphetamine and buprenorphine were injected intraperitoneal (i.p) for five days. To measure the analgesic threshold, the Tail-Flick test was used. Additionally, the real-time PCR technique was applied to evaluate the expression levels of AKT and GSK3b genes in the lumbar spinal cord of male rats. A one-way ANOVA test was used to analyze the data.
Results: Intraperitoneal injection of methamphetamine (10 mg/kg) induced analgesia (P < 0.05) and increased the expression of the gene of AKT (P < 0.05) in the lumbar spinal cord of male rats. In addition, the injection of buprenorphine (6 and 10 mg/kg) potentiated the effect of methamphetamine on analgesia (P < 0.01) and increased the expression of the GSK3b gene (P < 0.05), whereas the higher dose of buprenorphine reduced the impact of methamphetamine on the expression of AKT gene (P < 0.05). Furthermore, the deprivation of methamphetamine, did not alter Tail Flick latency and the expression level of AKT and GSK3b genes.
Conclusion: Our results indicated a possible reinforcing role of the buprenorphine on the increasing impact of acute methamphetamine injection on the expression of the GSK3b gene and analgesia.
Fariba Rasannezhad, Asieh Abbassi-Daloii , Seyyed Javad Ziaolhagh , Ahmad Abdi ,
Volume 11, Issue 1 (1-2024)
Abstract
Introduction: Methamphetamine addiction is one of the most prevalent substance use disorders. Augmenting traditional drug treatments with non-pharmacological interventions can enhance treatment efficacy and sustainability. This study aims to investigate the impact of aerobic exercise and psilocybin on histopathological changes in the cerebral cortex of methamphetamine-induced rats.
Material & Methods: This experimental research involved 30 female rats randomly allocated into five groups: control, methamphetamine, methamphetamine + aerobic exercise, methamphetamine + psilocybin, and methamphetamine + psilocybin + aerobic exercise. Rats received 15 mg of methamphetamine intraperitoneally every 12 hours for four days. Aerobic exercise was conducted on a treadmill with an 8-week program of escalating intensity, reaching a maximum running time of 30 minutes and speed of 25 m/min, with a 5% slope introduced in the fourth week. Psilocybin was administered intraperitoneally at a microdose of 0.025 mg/kg over 24 sessions. Histopathological changes were assessed using hematoxylin and eosin staining, and descriptive analysis with images was employed to interpret cortical brain tissue samples.
Results: Histological examination revealed tissue and cellular disorganization, altered morphology of pyramidal neurons, and reduced microglial cell counts in methamphetamine-induced rats compared to controls. Endurance training, psilocybin supplementation, and their combination exhibited improvements in tissue and cellular alterations in the cerebral cortex of addicted rats.
Conclusion: This study demonstrates that exercise training and psilocybin administration in methamphetamine-exposed rats ameliorate cortical histopathology, with the combined intervention yielding the most significant effects. This synergistic effect may reduce the risk of relapse in methamphetamine users by positively modulating brain and central nervous system functions.
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