Effects of environmental enrichment on behavior like depression and inflamatuar response in experimental vascular dementia models

Chronic cerabral hypoperfusion causes energy metabolism disorder, protein synthesis abnormalities, glial activation, apoptosis, oxidative stres, neuronal damage, inflammatory response. Experimental studies, environmental enrichment haas been found to show beneficial effects on aging, Alzheimer's disease and vascular dementia models. The aim of the this study was to determine the neuroprotective effect of environmental enrichment in chronic cerabral hypoperfusion by evaluating depression-like behavior and neuroinflammation. In our study, 30 male Wistar Albino rats were used. Chronic cerabral hypoperfusion was induced by bilateral carotid artery occlusion. Environmental enrichment was done for 4 weeks. Animals are divided in three groups; 1) Control group housed in standard cages without any treatment (n:10), 2) Chronic cerabral hypoperfusion group, housed in standard cages (n:10), 3) Chronic cerabral hypoperfusion+environmental enrichment group which exposed to environmental enrichment for 4 weeks (n:10). The sucrose preference test and force swimming test were used to evaluate depression-like behavior. BDNF, IL-1β and caspase-1 levels in hippocampus and cortex were measured by ELİSA. The differences between the groups were evaluated by Kruskal-Wallis and post-hoc Bonferroni test. It was determined that the duration of immobility of chronic cerabral hypoperfusion group increased in force swimming test and decreased after environmental enrichment exposure. It was determined that BDNF levels in the hippocampus increased significantly in the environmental enrichment group compared to the chronic cerabral hypoperfusion group. The levels of caspase-1 and IL-1β increased by chronic cerabral hypoperfusion, this increase was reduced by environmental enrichment exposure. As a result, environmental enrichment was effective in reducing depressive behavior after chronic cerabral hypoperfusion by reducing inflammatory response and preserving BDNF level in the hippocampus.