Related Experiment Videos
Temporal relationships between Ca2+ store mobilization and Ca2+ entry in an exocrine cell
1Department of Physiology, University of Rochester School of Medicine and Dentistry, New York.
Cell Calcium
|June 1, 1994
Summary
Capacitative models explain calcium (Ca2+) entry delays in non-excitable cells. Store depletion triggers an unknown messenger, activating Ca2+ entry pathways.
Area of Science:
- Cellular Biology
- Physiology
- Biochemistry
Background:
- Agonist-induced calcium (Ca2+) entry is crucial in non-excitable cells.
- Current models predict distinct temporal relationships between Ca2+ release and entry.
Purpose of the Study:
- To investigate the temporal dynamics of Ca2+ entry activation following agonist stimulation.
- To differentiate between existing models of Ca2+ entry in avian exocrine cells.
Main Methods:
- Measurements of intracellular Ca2+ ([Ca2+]i) and Mn2+ quench in individual avian exocrine cells.
- Stimulation with inositol trisphosphate (Ins(1,4,5)P3) and thapsigargin.
- Inhibition studies using SK&F 96365 and assessment of inositol tetrakisphosphate (Ins(1,3,4,5)P4) generation.
Main Results:
- Ins(1,4,5)P3-induced Ca2+ release occurred within 3-5 seconds.
- Mn2+ quench, reflecting Ca2+ entry, was delayed by 20-30 seconds.
- The delay was not caused by elevated [Ca2+]i or Ins(1,3,4,5)P4 generation.
Conclusions:
- The observed delay supports capacitative models of Ca2+ entry.
- Ca2+ entry activation requires a messenger generated by intracellular Ca2+ store depletion.
- This messenger is transmitted to the plasma membrane to activate entry pathways.