A kinetic model on calcium residues and facilitation.
The role of calcium as a regulator for neuronal function is very important. Calcium initiates many reactions that determine the behavior of the neuronal cell. In this article we use a kinetic model of the presynaptic synapsin I protein. This protein is responsible, via phosphorylation, for regulating the amount of transmitter vesicles available for release. This protein has been shown to inhibit the amount of vesicles ready for release in its dephosphorylated state, and releases its inhibitory binding due to phosphorylation. The phosphorylation of synapsin I depends on cyclic adenosine monophosphate and type II calcium/calmodulin protein kinase. Due to the duration of these two second messengers, we show that short-term facilitation does not have to depend on calcium residues. Furthermore, we show that calcium residues (in parts of microM range) promote increased facilitation due to the additional calcium reacting with the second messenger system.
Lundh
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Department of Computer Science, University of Skövde, Sweden. dan@ida.his.se
D000200:Action Potentials / Q000502:physiology; D002118:Calcium / Q000502:physiology*; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D017871:Calcium-Calmodulin-Dependent Protein Kinases / Q000378:metabolism; D002147:Calmodulin / Q000378:metabolism; D003198:Computer Simulation; D000242:Cyclic AMP / Q000378:metabolism; D007700:Kinetics; D008959:Models, Neurological; D009474:Neurons / Q000502:physiology*; D010766:Phosphorylation; D015290:Second Messenger Systems; D016704:Synapsins / Q000378:metabolism
D002147:Calmodulin; D016704:Synapsins; D000242:Cyclic AMP; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D017871:Calcium-Calmodulin-Dependent Protein Kinases; D002118:Calcium