Acute and Chronic Tramadol Treatment Impresses Tyrosine Kinase B (Trk-B) Receptor in the Amygdala and Nucleus Accumbens

Abstract

<strong>Background:</strong> Misuse of opioid painkillers such as tramadol has increased in the world. These painkillers have psychological side effects such as dependence and tolerance. Moreover, the role of Tyrosine-Kinase B (Trk-B) receptor in drug dependence and reward system is not clear. The main objective of the study is to assess the effect of tramadol on the Trk-B receptors within amygdala and nucleus accumbens.<br /><strong>Methods:</strong> For this purpose, the male Wistar rats received different doses of tramadol (0, 5, and 10 mg/kg). For the assessment of the effect of acute and chronic treatment of tramadol, animals received tramadol one and 14 following days, respectively. The amygdala and nucleus accumbens (NAC) were collected, and Trk-3 protein level was quantified using Western Blotting method. The collected results were subjected into statistical analysis using SPSS software.<br /><strong>Results:</strong> Results showed that Trk-B level increased in the amygdala in both acute and chronic treatment. Vice-versa, tramadol treatment decrease Trk-B level in the NAC.<br /><strong>Conclusion:</strong> Increasing of Trk-B level in the amygdala might be related to the effect of tramadol on serotonin reuptake transporter, and it proves the anxiolytic effect of tramadol. Decreasing in the level of Trk-B in the NAC might be related to the effect of tramadol on VTA and its rewarding effect via increasing dopamine in the NAC and decreasing Trk-B level in the D1-type Medium Spiny Neurons (MSN) which enhance reward., Increasing level of Trk-B in the amygdala might be related to the anxiolytic effect of tramadol which modulates it via BDNF-Trk-B signaling pathway. More studies are needed to elucidate the effect of tramadol on BDNF-TrkB signaling pathway.