MBI Publications

MBI Publications for Andrew Oster (9)

  • A. Oster and P. Bressloff
    Laminar network model for the joint development of ocular dominance columns and CO blobs in V1
    (In Preparation)

    Abstract

  • A. Oster, D. Terman and C. Fall
    . The mitochondrial permeability transition pore: modeling its formation through membrane-bound protein aggregation
    (In Preparation)

    Abstract

  • A. Oster, D. Terman and C. Fall
    Calcium interactions between the endoplasmic reticulum and mitochondria: the coupling of two excitable media
    (In Preparation)

    Abstract

  • A. Oster, P. Faure and B. Gutkin
    echanisms for multiple activity modes of midbrain DA neurons
    (In Preparation)

    Abstract

  • A. Oster and P. Bressloff
    A laminar network model for the joint development of ocular dominance columns and CO blobs in V1
    (In Preparation)

    Abstract

  • P. Bressloff and A. Oster
    A theory for the alignment of cortical feature maps during development
    Phys Rev E Stat Nonlin Soft Matter PhysVol. 82 No. 2 Pt 1 (2010)

    Abstract

  • A. Oster, B. Thomas, D. Terman and C. Fall
    The mitochondrial permeability transition pore confers excitability and CICR wave propagation
    J Theor BiolVol. 273 No. 1 (2011) pp. 216-31

    Abstract

  • A. Oster, B. Thomas, D. Terman and C. Fall
    The low conductance mitochondrial permeability transition pore confers excitability and CICR wave propagation in a computational model
    Journal of Theoretical BiologyVol. 273 No. 1 (2011) pp. 216-231

    Abstract

    Mitochondria have long been known to sequester cytosolic Ca(2+) and even to shape intracellular patterns of endoplasmic reticulum-based Ca(2+) signaling. Evidence suggests that the mitochondrial network is an excitable medium which can demonstrate independent Ca(2+) induced Ca(2+) release via the mitochondrial permeability transition. The role of this excitability remains unclear, but mitochondrial Ca(2+) handling appears to be a crucial element in diverse diseases as diabetes, neurodegeneration and cardiac dysfunction that also have bioenergetic components. In this paper, we extend the modular Magnus-Keizer computational model for respiration-driven Ca(2+) handling to include a permeability transition based on a channel-like pore mechanism. We demonstrate both excitability and Ca(2+) wave propagation accompanied by depolarizations qualitatively similar to those reported in cell and isolated mitochondria preparations. These waves depend on the energy state of the mitochondria, as well as other elements of mitochondrial physiology. Our results support the concept that mitochondria can transmit state dependent signals about their function across the mitochondrial network. Our model provides the tools for predictions about the internal physiology that leads to this qualitatively different Ca(2+) excitability seen in mitochondria.
  • A. Oster and B. Gutkin
    A reduced model of DA neuronal dynamics that displays quiescence, tonic firing, and bursting
    J. Physiol. (2011)

    Abstract

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