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Related Experiment Videos

Receptor-regulated calcium entry.

J W Putney1

  • 1Calcium Regulation Section, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709.

Pharmacology & Therapeutics
|January 11, 1990
PubMed
Summary
This summary is machine-generated.

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Cellular responses involve calcium (Ca2+) mobilization from internal stores and extracellular entry. Depletion of intracellular Ca2+ stores, triggered by D-myo-inositol 1,4,5-trisphosphate, activates Ca2+ entry.

Area of Science:

  • Cellular Biology
  • Molecular Physiology
  • Signal Transduction

Background:

  • Hormones and neurotransmitters trigger cellular responses by mobilizing intracellular calcium (Ca2+).
  • This Ca2+ mobilization involves release from intracellular stores and influx from the extracellular space.
  • D-myo-inositol 1,4,5-trisphosphate is a key second messenger mediating intracellular Ca2+ release.

Purpose of the Study:

  • To elucidate the mechanisms of Ca2+ entry into the cytoplasm.
  • To investigate the role of inositol polyphosphates in activating Ca2+ entry.
  • To test the capacitative model for Ca2+ entry.

Main Methods:

  • Utilizing diverse experimental strategies to investigate Ca2+ mobilization.
  • Manipulating intracellular Ca2+ pool levels.

Related Experiment Videos

  • Assessing Ca2+ entry under conditions of varying receptor activation and inositol polyphosphate levels.

    • Main Results:

    • Depletion of intracellular Ca2+ stores activates Ca2+ entry.
    • This activation occurs independently of receptor activation.
    • Ca2+ entry can be triggered by store depletion even without elevated inositol polyphosphates.

    Conclusions:

    • The capacitative model provides a framework for understanding Ca2+ entry.
    • Intracellular Ca2+ store depletion is a critical signal for activating Ca2+ influx.
    • The precise mechanism linking inositol polyphosphates to Ca2+ entry requires further investigation.