• DocumentCode
    380167
  • Title

    Model of Ca2+ concentration controlled by sarcoplasmic reticulum of skeletal muscle, using the state transition

  • Author

    Yokota, M. ; Yokota, Y.

  • Author_Institution
    Fac. of Inf. & Culture, Nagoya Bunri Univ., Aichi, Japan
  • Volume
    3
  • fYear
    2001
  • fDate
    2001
  • Firstpage
    2967
  • Abstract
    [Ca2+] in a muscle cell is controlled by the sarcoplasmic reticulum (SR) that releases Ca2+ through the channels, takes up Ca2+ by the pumps on the SR membrane, and stores up Ca2+ with Ca2+ binding protein called calsequestrin (CS). This report proposed a model that represents [Ca2+] in a muscle cell controlled by the SR using a state transition probability model in which one state means that protein in the SR is binding ligands, and the other is releasing them. The proposed model consists of 4 modules: calsequestrin, voltage dependent Ca2+ release channels, Ca2+ induced Ca2+ release channels, and Ca2+ pumps. Estimating the amount of Ca2+ both released and pumped up with the model, it was indicated that [Ca2+] rapidly increases from the static state as soon as nerve impulses arrive at a muscle. We further reveal that the fact that Ca2+ pumps are located apart from Ca2+ release channels has an important influence on generating a Ca2+ spike signal.
  • Keywords
    biocontrol; bioelectric potentials; biomembrane transport; calcium; muscle; neurophysiology; proteins; Ca2+; Ca2+ concentration model; Ca2+ induced Ca2+ release channels; Ca2+ pumps; Ca2+ spike signal; SR membrane; binding protein; calsequestrin; ligand binding; muscle cell; nerve impulses; protein; sarcoplasmic reticulum; skeletal muscle; state transition probability model; static state; voltage dependent Ca2+ release channels; Biomembranes; Chemicals; Equations; Force control; Muscles; Optical fiber sensors; Proteins; Stochastic processes; Strontium; Voltage control;
  • fLanguage
    English
  • Publisher
    ieee
  • Conference_Titel
    Engineering in Medicine and Biology Society, 2001. Proceedings of the 23rd Annual International Conference of the IEEE
  • ISSN
    1094-687X
  • Print_ISBN
    0-7803-7211-5
  • Type

    conf

  • DOI
    10.1109/IEMBS.2001.1017415
  • Filename
    1017415