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A kinetic model on calcium residues and facilitation
University of Skövde, Department of Computer Science. (Biocomputing Group)ORCID iD: 0000-0002-6549-086X
1998 (English)In: Brain Research Bulletin, ISSN 0361-9230, E-ISSN 1873-2747, Vol. 45, no 6, p. 589-597Article in journal (Refereed) Published
Abstract [en]

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 μM range) promote increased facilitation due to the additional calcium reacting with the second messenger system.

Place, publisher, year, edition, pages
Elsevier, 1998. Vol. 45, no 6, p. 589-597
Keywords [en]
Phosphorylation, Synapsin I, cAMP, CaM kinase II, Facilitation
Identifiers
URN: urn:nbn:se:his:diva-2383DOI: 10.1016/S0361-9230(97)00456-5ISI: 000072972400008PubMedID: 9566503Scopus ID: 2-s2.0-0032053135OAI: oai:DiVA.org:his-2383DiVA, id: diva2:126879
Available from: 2008-11-25 Created: 2008-11-25 Last updated: 2017-12-15Bibliographically approved

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Lundh, Dan

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