Resumo

Studies have shown that an enriched environmental (EE) enhances hippocampal neurogenesis and dendritic branching in rodents, improving the performance in learning and memory task. Diabetes (D), however, is associated with memory deficits and decreasing in cell proliferation in the hippocampal dentate gyrus (DG), possibly related with higher glucocorticoid levels. Thus, our objective was to investigate the influence of EE on the memory deficits and cell proliferation of diabetic rats. For this, 41 Wistar male rats were reared for 2 months during early stages of life in standard environments (control rats, C) or EE. At adulthood, control and EE groups were divided and half of them induced to diabetes by a single injection of streptozotocin, 60 mg/kg, i.p. Non-diabetic rats (ND) were injected only with citrate buffer, 1 ml/Kg, i.p. Memory deficit was evaluated in these groups in the novel object-placement recognition task 11 days after diabetes induction. BrdU label cells were detected by immunohistochemistry after 3 days of administration to correlate cell proliferation in the DG area and performance in the memory task. The data were analyzed using two-way ANOVA and Student-Newman-Keuls post hoc test. Data were expressed as mean ± S.E.M. Our results showed that EE decreased memory deficits in diabetic-induced rats (percentage of preference for exploring the relocated object: NDC 57.58 ± 3.74; DC 41.96 ± 6.35%; DEE 63.09 ± 8.76; NDEE 73.52 ± 3.45%; p<0.05). Although cell proliferation in the DG was lower in the diabetic rats (p=0.01), enriched environment did not interfere in this parameter (number of BrdU-labeled cell in the DG: NDC 32.1 ± 3.75; DC 22.8 ± 3.84; NDEE 33.55 ± 3.21; DEE: 23.62 ± 2.33). These findings suggest that enriched environment is able to prevent the development of memory deficits caused by diabetes in rats.