Aging increases calcium influx at motor nerve terminal

To determine whether increased transmitter release from soleus nerve terminals of old C57BL/6J mice is caused by an altered Ca²⁺ regulation, the time course of post-tetanic potentiation of miniature endplate potential (MEPP) frequency was used as an indicator of the kinetics of Ca²⁺ metabolism in young (10 months) and old (24 months) mice. Post-tetanic potentiation properties were studied in either (1) 0.2 mM Ca²⁺, 5.0 mM Mg²⁺ Krebs; or (2) Ca²⁺-free/EGTA Krebs to eliminate Ca²⁺ influx, and thereby isolated Ca²⁺ buffering. In the 0.2 mM Ca²⁺ Krebs, the time constants of decay of augmentation (T_A) and potentiation (T_P) were longer in old (T_A = 10.3 ± 1.0 sec, T_P = 195.3 ± 5.4 sec) than in young (T_A = 7.0 ± 0.7 sec, T_P = 78.8 ± 6.6 sec) nerve terminals. Evoked transmitter release was measured in 0.4 mM Ca²⁺, 2.75 mM Mg²⁺ Krebs. Quantal content of the endplate potential was positively correlated with T_A (r = 0.95) and with T_P (r = 0.98). In the Ca²⁺-free/EGTA Krebs, there was no difference in post-tetanic potentiation properties between young and old terminals. These results suggest that Ca²⁺ influx into the soleus nerve terminal increases with aging. This may explain, at least in part, the increased quantal content observed at old terminals.