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Related Experiment Videos

Endoplasmic reticulum calcium release is modulated by actin polymerization.

Yue Wang1, Mark P Mattson, Katsutoshi Furukawa

  • 1Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, Baltimore, Maryland 21224, USA.

Journal of Neurochemistry
|October 3, 2002
PubMed
Summary

The actin cytoskeleton regulates calcium release from intracellular stores in neurons. Disrupting actin filaments reduces calcium release, while polymerizing them enhances it, impacting neuronal cell death.

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Biochemistry

Background:

  • Intracellular calcium ions are crucial regulators of cytoskeletal protein structure and function.
  • The cytoskeleton, particularly actin filaments, influences calcium influx via plasma membrane channels.

Purpose of the Study:

  • To investigate the role of actin filament polymerization and depolymerization in modulating calcium release from endoplasmic reticulum (ER) stores in cultured hippocampal neurons.

Main Methods:

  • Treatment of cultured hippocampal neurons with actin-depolymerizing agent (cytochalasin D) or actin-polymerizing agent (jasplakinolide).
  • Measurement of calcium release induced by various agonists (carbamylcholine, caffeine, thapsigargin) in the presence and absence of extracellular calcium.
  • Assessment of JNK activation and neuronal cell death following thapsigargin treatment.

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Main Results:

  • Depolymerization of actin filaments with cytochalasin D attenuated calcium release from IP3 and ryanodine-sensitive ER stores.
  • The actin-polymerizing agent jasplakinolide potentiated calcium release induced by IP3 and ryanodine receptor agonists.
  • Cytochalasin D reduced, while jasplakinolide increased, thapsigargin-induced JNK activation and neuronal cell death.

Conclusions:

  • The actin cytoskeleton plays a significant role in regulating calcium release from intracellular ER stores.
  • Actin's modulation of ER calcium release suggests its involvement in physiological and pathological processes linked to calcium signaling.