BACKGROUND: A growing body of evidence has shown an association between diabetes and depression, as well a role of brain-derived neurotrophic factor (BDNF) in diabetes and depression. The present study was designed to evaluate the behavioural and molecular effects of the anti-depressant imipramine in diabetic rats. METHODS: To this aim, after induction of diabetes by alloxan (150 mg/kg), Wistar rats were treated with imipramine (30 mg/kg) once a day for 14 days and then subjected to behavioural tests. BDNF was then assessed in the prefrontal cortex, hippocampus and amygdala. RESULTS: In diabetic rats treated with saline, we observed an increase in the immobility time, compared with control rats treated with saline. Treatment with imipramine decreased the immobility time in nondiabetic and diabetic rats, compared with both nondiabetic and diabetic rats treated with saline. In the open-field test, it was observed that treatment with imipramine reduced the number of crossings the diabetic rats performed, compared with nondiabetic rats treated with saline. The number of rearings did not alter in any of the groups. Diabetic rats injected with saline did not show altered BDNF levels in the prefrontal cortex, hippocampus or amygdala, but interestingly, the treatment with imipramine in diabetic animals increased BDNF levels in the prefrontal cortex. CONCLUSIONS: In conclusion, this study demonstartes a link between diabetes and depression in rats and that imipramine exerted antidepressant effects in diabetic animals.
BACKGROUND: A growing body of evidence has shown an association between diabetes and depression, as well a role of brain-derived neurotrophic factor (BDNF) in diabetes and depression. The present study was designed to evaluate the behavioural and molecular effects of the anti-depressant imipramine in diabeticrats. METHODS: To this aim, after induction of diabetes by alloxan (150 mg/kg), Wistar rats were treated with imipramine (30 mg/kg) once a day for 14 days and then subjected to behavioural tests. BDNF was then assessed in the prefrontal cortex, hippocampus and amygdala. RESULTS: In diabeticrats treated with saline, we observed an increase in the immobility time, compared with control rats treated with saline. Treatment with imipramine decreased the immobility time in nondiabetic and diabeticrats, compared with both nondiabetic and diabeticrats treated with saline. In the open-field test, it was observed that treatment with imipramine reduced the number of crossings the diabeticrats performed, compared with nondiabetic rats treated with saline. The number of rearings did not alter in any of the groups. Diabeticrats injected with saline did not show altered BDNF levels in the prefrontal cortex, hippocampus or amygdala, but interestingly, the treatment with imipramine in diabetic animals increased BDNF levels in the prefrontal cortex. CONCLUSIONS: In conclusion, this study demonstartes a link between diabetes and depression in rats and that imipramine exerted antidepressant effects in diabetic animals.
Authors: Taise Possamai-Della; Gustavo C Dal-Pont; Wilson R Resende; Jorge M Aguiar-Geraldo; Jefté Peper-Nascimento; João Quevedo; Samira S Valvassori Journal: Mol Neurobiol Date: 2022-09-19 Impact factor: 5.682
Authors: Luciane B Ceretta; Gislaine Z Réus; Helena M Abelaira; Karine F Ribeiro; Giovanni Zappellini; Francine F Felisbino; Amanda V Steckert; Felipe Dal-Pizzol; João Quevedo Journal: Exp Diabetes Res Date: 2012-05-08