Background & Aim: Any disturbance in the function of central aminergic system is the main cause of depression in diabetes. Since most of the available antidepressants have limitations, it is necessary to research other options of treatment. The purpose of this study was the investigation of the possible antidepressant effect of melatonin on diabetic rats.
Material and Method: This experimental study involved 40 male Wistar rats weighing 200±20 gr. The animals were divided into four groups: control, melatonin, diabetic, and melatonin-treated diabetic. Experimental diabetes was induced by intraperitoneal (i.p.) injection of 50 mg/kg streptozotocin. 72 hours after diabetes induction, melatonin (10 mg/kg/day, i.p.) was injected for 5 weeks. At the end of administration period, the modified forced swimming test (MFST) and the open-field test were used for evaluation of depression and its possible mechanism. The MFST evaluated climbing, swimming and immobility periods and the locomotor activity was evaluated by the open-field test. The experimental data were statistically analyzed by one-way analysis of variance (ANOVA) followed by Tukey test, using the software package SPSS v.15.
Results: The swimming test shows that diabetes causes a significant (p<0.05) increase in immobility and climbing periods (as depression and noradrenergic system activity indices respectively) as compared with the control group. The swimming time (as serotonergic system activity index) and the locomotor activity (as dopaminergic system activity index) were significantly (p<0.05) decreased in diabetic rats as compared with the control group. Daily melatonin injection to diabetic rats significantly (p<0.05) modified all mentioned behavioral indices as compared with the diabetic group. Melatonin significantly (p<0.05) decreased the locomotor activity in non-diabetic rats as compared with the control group, whereas it did not have any significant effects on swimming, climbing or immobility periods in these animals.
Conclusion: Melatonin has antidepressant effects in diabetes through modifying central aminergic system.
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