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Related Experiment Videos

Osmotic forces and gap junctions in spreading depression: a computational model.

B E Shapiro1

  • 1Machine Learning Systems Group, Jet Propulsion Laboratory, California Institute of Technology, Pasadena 91109, USA. bshapiro@jpl.nasa.gov

Journal of Computational Neuroscience
|April 24, 2001
PubMed
Summary
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Computational models reveal spreading depression (SD) requires cell expansion and potassium (K+) movement through gap junctions. This research clarifies key mechanisms driving SD propagation in the brain.

Area of Science:

  • Computational neuroscience
  • Neurophysiology
  • Biophysics

Background:

  • Spreading depression (SD) is a wave of neuronal depolarization with implications for neurological disorders.
  • The precise ionic and cellular mechanisms driving SD propagation remain incompletely understood.
  • Previous models have not fully integrated cellular volume changes and gap junction dynamics.

Purpose of the Study:

  • To develop and analyze a computational model of spreading depression (SD) incorporating electrodiffusion, cellular volume changes, and gap junction coupling.
  • To identify critical factors necessary for the initiation and propagation of SD waves.
  • To compare model predictions with experimental observations of SD.

Main Methods:

  • Electrodiffusive modeling of ionic movement within a neuronal syncytium connected by gap junctions.

Related Experiment Videos

  • Inclusion of cell volume changes in response to osmotic pressure gradients.
  • Parametric analysis across ranges reported for gray matter.

    • Main Results:

    • SD propagation necessitates cell expansion and potassium (K+) movement through gap junctions.
    • Simulations predict SD waves with extracellular K+ ([K+]out) of 25–60 mM and speeds of 2–18 mm/min.
    • Extracellular space reduction up to 50% was predicted, consistent with experimental findings.
    • Specific ion currents (delayed-rectifier, NMDA, BK, Na+) facilitate SD, while others (SK, A-type K+) and glial activity impede it.

    Conclusions:

    • Cytosolic diffusion via gap junctions and osmotic forces are crucial mechanisms underlying SD.
    • Model predictions align with experimental data, including the effects of gap junction blockers.
    • The study provides a mechanistic framework for understanding SD propagation and its modulation.