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Aging increases calcium influx at motor nerve terminal
1Andrus Gerontology Center, University of Southern California, Los Angeles 90089-0191.
Summary
Aging increases calcium influx into mouse nerve terminals, leading to enhanced transmitter release. This study investigated calcium regulation changes in old mice, finding altered potentiation kinetics linked to increased quantal content.
Area of Science:
- Neuroscience
- Aging Research
- Calcium Signaling
Background:
- Aging is associated with altered neurotransmission.
- Increased transmitter release is observed in aged soleus nerve terminals.
- The role of calcium (Ca2+) regulation in age-related changes in neurotransmission requires further investigation.
Purpose of the Study:
- To investigate whether increased transmitter release in aged soleus nerve terminals is due to altered Ca2+ regulation.
- To examine the kinetics of Ca2+ metabolism in young and old mice using post-tetanic potentiation (PTP) of miniature endplate potential (MEPP) frequency.
Main Methods:
- Studied PTP properties in young (10 months) and old (24 months) C57BL/6J mice soleus nerve terminals.
- Utilized Krebs solutions with varying Ca2+ and Mg2+ concentrations, including Ca2+-free/EGTA conditions to isolate Ca2+ buffering.
- Measured evoked transmitter release and correlated quantal content with PTP time constants (TA and TP).
Main Results:
- Time constants of augmentation (TA) and potentiation (TP) decay were significantly longer in old mice compared to young mice.
- Quantal content of the endplate potential showed a strong positive correlation with both TA and TP.
- No differences in PTP properties were observed between young and old terminals in Ca2+-free/EGTA conditions.
Conclusions:
- Altered Ca2+ regulation, specifically increased Ca2+ influx into the soleus nerve terminal, occurs with aging.
- This age-related increase in Ca2+ influx likely contributes to the enhanced quantal content observed in aged nerve terminals.