Dresden 2006 – wissenschaftliches Programm

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AKB: Biologische Physik

AKB 40: Poster Session II

AKB 40.57: Poster

Mittwoch, 29. März 2006, 16:30–19:30, P3

Transitions in a bistable model of the calcium/calmodulin-dependent protein kinase-phosphatase system in response to LTP and LTD protocols — •Michael Graupner and Nicolas Brunel — Laboatoire de Neurophysique et Physiologie, CNRS UMR 8119, Université René Descartes - Paris V, Paris, France

The calcium/calmodulin-dependent protein kinase II (CaMKII) plays a key role during induction of long-term post-synaptic modifications following calcium entry. The biochemical network involving CaMKII and its regulating protein signaling cascade has been hypothesized to be a bistable realization of such a switch. However, it is still unclear whether LTP/LTD protocols lead to transitions between these two states in realistic models of such a network. A detailed biochemical model of the CaMKII autophosphorylation and the protein signaling cascade governing the CaMKII dephosphorylation is presented. As reported by Zhabotinsky [Biophys J 2000; 79:2211], two stable states of such a system exist at resting intracellular Ca(2+) concentration: a weakly-(DOWN) and a highly-phosphorylated (UP) state of the CaMKII. A transition from the DOWN to the UP state can be achieved by high calcium elevations. Intermediate Ca(2+) concentrations enhance CaMKII dephosphorylation. This results in depotentiation - switching from the UP to the DOWN. Finally, it is shown that the CaMKII system can qualitatively reproduce results of plasticity outcomes in response to standard experimental induction paradigms of long-term modifications.