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 (TA) and potentiation (TP) were longer in old (TA = 10.3 +/- 1.0 sec, TP = 195.3 +/- 5.4 sec) than in young (TA = 7.0 +/- 0.7 sec, TP = 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 TA (r = 0.95) and with TP (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.