Abstract
Introduction: Aripiprazole is a partial agonist of dopamine D2 and D3 and serotonin 5-HT1A, 5-HT2C and 5-HT7 receptors, and it is also an antagonist of serotonin 5-HT2A and 5-HT6 receptors. Partial D2 receptor agonism is thought to stabilize dopaminergic neurotransmission in the mesolimbic and mesocortical pathways. Dysregulation in the dopamine and serotonin systems is known to be one of the factors that is responsible for the etiology of depression. In this study, we aimed to evaluate the antidepressant potential of aripiprazole in rats by studying its effects on dopamine and serotonin receptors.Method: In this study, male Wistar Albino rats of 8-week old were used. They were divided into 4 groups, each of which consisted of 8 rats. As a depression model, the Chronic Mild Stress (CMS) model was used for four weeks on the rats. The first group was the control group and that received saline as a placebo without CMS. For the second group, aripiprazole (2.5 mg/kg) was administered with CMS; for the third group, escitalopram (10mg/kg) was administered with CMS and for fourth group a placebo (serum physiologic) was given with CMS. Additionally a sucrose consumption test was performed before and after the CMS model.Results: Sucrose intake at the baseline and within the first week of the study did not differ among the groups. The sucrose consumption of the group with CMS was significantly lower than that of the control group during the second, third and fourth weeks. While the consumption of sucrose in the groups who received aripiprazole and escitalopram did not differ from the group which was exposed to CMS at the beginning and during the first and second weeks, it was significantly higher at the third and fourth weeks. The sucrose consumption values of the groups that received aripiprazole and escitalopram were not different from the control group throughout the study.Conclusion: In this study, aripiprazole has been shown to produce an antidepressant effect comparable to that of escitalopram in rats using a model of depression.
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More From: Klinik Psikofarmakoloji Bülteni-Bulletin of Clinical Psychopharmacology
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