Aging increases calcium influx at motor nerve terminal

Waleed B. Alshuaib, Mohamed A. Fahim

Research output: Contribution to journalArticlepeer-review

18 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)655-666
Number of pages12
JournalInternational Journal of Developmental Neuroscience
Issue number6
Publication statusPublished - 1990
Externally publishedYes


  • Ca homeostasis
  • aging
  • neuromuscular transmission
  • post-tetanic potentiation
  • synaptic plasticity

ASJC Scopus subject areas

  • Developmental Neuroscience
  • Developmental Biology


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