In vitro aging reduces the morphological plasticity of astrocytes

Abstract Astrocytes are involved in many functions of the brain including water transport and moderation of neuronal synapses, and most functions require the astrocyte endfeet to be highly mobile. In the aging brain the functions in the brain start to deteriorate, decay or loss of metabolic functions may eventually cause diseases such as Parkinsons’s and Alzheimer’s disease. In this study cAMP-induced stellation is used to observe how senescence affects the morphological plasticity of primary astrocytes. Morphological plasticity is a key factor in determining the mobility of an astrocyte and therefore the ability of an astrocyte to function. In addition, actin breakdown and aquaporin-4 (AQP4) movement are also investigated. We used later passaged astrocytes to show that astrocytes have lower percent stellation as a function of passage number. Results showed that astrocytes in later passages have a lower percent stellation than those in earlier passages. Also, early passages maintained stellated astrocytes for a longer time period of time. In addition two types of cAMP were used to compare how either affected stellation. Astrocytes incubated in the non-hydrolysable cAMP had a higher percent stellation than astrocytes in regular cAMP. Actin depolymerization and focal adhesion points were observed with stellated cells, and AQP4 stain was seen to localize at the endfeet processes. Experiments suggest that the reduced plasticity of aged astrocytes in the brain may contribute to the decreased ability of the cell to function properly, and imply a connection to age-related reduction of brain function.