MBI Publications

MBI Publications for David Terman (19)

  • J. Best, C. Park, C. Wilson and D. Terman
    Transitions between irregular and rhythmic firing patterns in an excilatory-inhibitory neuronal netowrk
    Journal of Computational Neuroscience

    Abstract

  • G. Enciso, A. Dmitriev, D. Terman and S. Mangel
    A mathematical model of signal propagation in the starburst amacrine cell network
    (Submitted)

    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

  • M. Rempe, A. Dmitriev, K. Gavrikov, D. Terman and S. Mangel
    A Morphologically-Accurate Model of Direction Selectivity in the Starburst Amacrine Cell Network
    (In Preparation)

    Abstract

  • M. Rempe, J. Best and D. Terman
    A Neurobiological Model of the Human Sleep/Wake Cycle
    MBI Technical Report No. 72

    Abstract

  • J. Best, A. Borisyuk, J. Rubin, D. Terman and M. Wechselberger
    The dynamic range of bursting in a network of synaptically coupled square-wave bursting respiratory pacemaker cells
    SIAM J. of Appl. Dyn. Syst.Vol. 4 (2005) pp. 1107-1139

    Abstract

  • J. Best, A. Borisyuk, J. Rubin, D. Terman and M. Wechselberger
    The dynamic range of bursting in a model respiratory pacemaker network
    SIAM Journal of Applied Dynamical SystemsVol. 4 (2005) pp. 1107-1139

    Abstract

  • J. Best, A. Borisyuk, J. Rubin, D. Terman and M. Wechselberger
    The Dynamic range of bursting in a model respiratory pacemaker network
    SIAM Journal on Applied Dynamical SystemsVol. 4 (2005) pp. 1107-1139

    Abstract

  • J. Best and D. Terman
    Geometric analysis of bursting networks
    World ScientificVol. Bursting: The Genesis of Rhythm in the Nervou (2005) pp. 351-386

    Abstract

  • Y. Guo, J. Rubin, C. McIntyre, J. Vitek and D. Terman
    Thalamocortical Relay Fidelity Varies Across Subthalamic Nucleus Deep Brain Stimulation Protocols in a Data-Driven Computational Model
    J. NeurophysiolVol. 99 (2008) pp. 1477-1492

    Abstract

  • M. Rempe, J. Best and D. Terman
     A Neurobiological Model of the Human Sleep/Wake Cycle
    J Math BiolVol. 60 (2009) pp. 615-644

    Abstract

  • G. Enciso, M. Rempe, A. Dmitriev, K. Gavrikov, D. Terman and S. Mangel
    A Model of Direction Selectivity in the Starburst Amacrine Cell Network
    J Comput Neurosci.Vol. 28 No. 3 (2010) pp. 567-578

    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.
  • M. Rempe, J. Best and D. Terman
    A Mathematical Model of the sleep/wake cycle
    J Math BiolVol. 60 (2012) pp. 615-644

    Abstract

  • S. Ahn, B. Smith, A. Borisyuk and D. Terman
    Analyzing Neuronal Networks Using Discrete-Time Dynamic
    Physica D: Nonlinear phenomenaVol. 239 No. 9 (2012) pp. 515-528

    Abstract

  • C. Diekman, C. Fall, J. Lechleiter and D. Terman
    Modeling the neuroprotective role of enhancing astrocyte mitochondrial metabolism during stroke
    Biophysical Journal (2013) (In Press)

    Abstract

    A mathematical model that integrates the dynamics of cell membrane potential, ion homeostasis, cell volume, mitochondrial ATP production, mitochondrial and ER Ca2+ handling, IP3 production and GTP-binding protein coupled receptor (GPCR) signaling was developed. Simulations with this model support recent experimental data showing a protective effect of stimulating an astrocytic GPCR (P2Y1Rs) following cerebral ischemic stroke. The model was analyzed in order to better understand the mathematical behavior of the equations and to provide insights into the underlying biological data. This approach yielded explicit formulas determining how changes in IP3-mediated Ca2+ release, under varying conditions of oxygen and the energy substrate pyruvate, affected mitochondrial ATP production, and was utilized to predict rate-limiting v
  • C. Diekman, C. Fall, J. Lechleiter and D. Terman
    Modeling the neuroprotective role of enhanced astrocyte mitochondrial metabolism during stroke.
    Biophysical journalVol. 104 No. 8 (2013) pp. 1752-63

    Abstract

    A mathematical model that integrates the dynamics of cell membrane potential, ion homeostasis, cell volume, mitochondrial ATP production, mitochondrial and endoplasmic reticulum Ca(2+) handling, IP3 production, and GTP-binding protein-coupled receptor signaling was developed. Simulations with this model support recent experimental data showing a protective effect of stimulating an astrocytic GTP-binding protein-coupled receptor (P2Y1Rs) following cerebral ischemic stroke. The model was analyzed to better understand the mathematical behavior of the equations and to provide insights into the underlying biological data. This approach yielded explicit formulas determining how changes in IP3-mediated Ca(2+) release, under varying conditions of oxygen and the energy substrate pyruvate, affected mitochondrial ATP production, and was utilized to predict rate-limiting variables in P2Y1R-enhanced astrocyte protection after cerebral ischemic stroke.

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