Ca2+ signalling pathways activated by acetylcholine in mouse C2C12 myotubes

Area of Science:

• Muscle physiology
• Cellular signaling
• Calcium homeostasis

Background:

• Acetylcholine (ACh) is a key neurotransmitter involved in muscle contraction.
• ACh elevates intracellular calcium ([Ca2+]i) in myotubes through various mechanisms.
• Understanding the sources of ACh-induced calcium increase is crucial for muscle function.

Purpose of the Study:

• To quantify the relative contributions of different calcium sources to ACh-induced [Ca2+]i elevation in mouse C2C12 myotubes.
• To investigate the presence of ACh-induced calcium mobilization in embryonic chick myotubes.
• To discuss the significance of distinct calcium signaling pathways during myogenesis.

Main Methods:

• Utilized mouse C2C12 myotubes as a model system.
• Measured myoplasmic Ca2+ ([Ca2+]i) concentrations.
• Differentiated calcium influx from internal calcium store mobilization.

Main Results:

• Calcium influx via voltage-gated and ACh-gated channels accounted for approximately 80% of the [Ca2+]i increase.
• Mobilization from internal caffeine- and inositol trisphosphate- (InsP3-) sensitive stores contributed the remaining 20%.
• ACh-induced mobilization from InsP3-sensitive stores was also observed in embryonic chick myotubes.

Conclusions:

• Extracellular calcium influx is the predominant source of ACh-evoked [Ca2+]i elevation in mature myotubes.
• Internal calcium stores play a significant, albeit smaller, role in this process.
• Similar calcium signaling mechanisms involving InsP3-sensitive stores are present during early myogenesis in different species.