Receptor medicated activation of many cell types is followed by motility related events. In T lymphocytes, lateral redistribution of surface receptors is accompanied by aggregation of action and myosin in cytoplasmic subcaps. Patching and capping of receptors after activation of lymphocytes from aged animals and humans is impaired, and it was inferred from indirect evidence that age-related changes in cytoskeletal functions are responsible. Concanavalin A activation of resting T lymphocytes resulted in actin polymerization in the cytoskeleton of cells from young but not aged C57BL/6 mice. Bypassing the plasma membrane to activate protein kinase C with PMA induced actin polymerization in resting T lymphocytes and in immunomagnetically isolated CD4 and CD8 positive subpopulations from young and aged mice. A higher percentage of F-actin subcaps in unstimulated CD8 positive cells from aged mice was seen than in all other groups. After activation with PMA, fewer young F-actin subcaps formed in both CD4 and CD8 positive cells from aged compared to young animals and their morphology differed from that of cells from young mice. This suggests that although plasma membrane signalling events are bypassed and actin polymerization is initiated in cells from aged mice, the function/s of F-actin change with age. Since T lymphocytes activated with Concanavalin A exhibit circannual rhythms in proliferation and their properties change with age, levels of polymerized actin in resting T lymphocytes and CD4 and CD8 positive cells stimulated with PMA were analyzed for seasonality in responses. Actin polymerized in spring and summer but not during winter months in cells from young mice, and there were no seasonal changes in cells from aged animals. F- actin levels were significantly higher in spring and summer and lower during winter in cells from young compared to aged mice. Therefore, seasonality in lymphocyte functions can obscure age-related defects, and, even though plasma membrane activation events are bypassed, subsequent signal transduction is impaired with age and during the winter season in cells from young animals.
