Can Social Instability, Food Deprivation and Food Inequality Accelerate Neuronal Aging?

Based on both animal and human studies, inequality in food intake and social instability has adverse effects on the health of individuals and the community. however, it is not known whether social instability, food deprivation and food inequality affect neuronal death and premature aging in young animals. to address this question, the effects of these adverse situations, histopathological changes in hippocampal pyramidal cells and aging process were investigated. forty eight new zeeland white male rabbits were divided into six groups and all of them were housed in similar conditions, with 2 animals per cage in a temperaturecontrolled colony room under light-dark cycle. all experimental animals were fed on standard rabbit commercial pellets and different social situations such as food deprivation, inequality in food intake, and unstable social status were applied to experimental groups during eight weeks. afterward, lipofuscin accumulation and apoptosis, as main markers of aging, were compared to the control group by long ziehl nelseen staining and the terminal deoxynucleotidyl transferase dutp nick end labeling (tunel reaction) assay to reveal the rate of lipofuscin pigment accumulation and tunel-reactive apoptotic bodies in the hippocampal pyramidal cells. serum cortisol level was also measured. inequality in social situation raised chronic stress (i.e. food deprivation, social inequality and instability) and caused significant changes in lipofuscin accumulation in hippocampal pyramidal cells in comparison to the control group (p<0.005). the results also showed a significant increase in the ratio of apoptotic to normal cells in all of the stressed groups compared to the control group (p<0.05). moreover, application of the social inequality and stresses alone or together modulated levels of cortisol in the experimental group. these findings suggest that food deprivation, inequality and social instability enhance the susceptibility of hippocampal pyramidal cells to apoptosis and premature aging induced by lipofuscin accumulation.