Models that contain the Modeling Application : Virtual Cell (Home Page)

(NRCAM, the National Resource for Cell Analysis and Modeling is developing a unique software modeling environment, the Virtual Cell, for quantitative cell biological research. NRCAM is currently funded through the NCRR, National Center for Research Resources, a component of the National Institutes of Health (NIH).)
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    Models   Description
1.  A nicotinic acetylcholine receptor kinetic model (Edelstein et al. 1996)
Nicotinic acetylcholine receptors are transmembrane oligomeric proteins that mediate interconversions between open and closed channel states under the control of neurotransmitters. .. In order to represent the functional properties of such receptors, we have developed a kinetic model that links conformational interconversion rates to agonist binding and extends the general principles of the Monod- Wyman-Changeux model of allosteric transitions. ... Application of the model to the peripheral nicotinic acetylcholine receptor (nAChR) accounts for the main properties of ligand-gating, including single-channel events, and several new relationships are predicted. ... In terms of future developments, the analysis presented here provides a physical basis for constructing more biologically realistic models of synaptic modulation that may be applied to artificial neural networks.
2.  Calcium waves in neuroblastoma cells (Fink et al. 2000)
Uses a model of IP3-mediated release of Ca from endoplasmic reticulum (ER) to study how initiation and propagation of Ca waves are affected by cell geometry, spatial distributions of ER and IP3 generation, and diffusion of Ca and mobile buffer.
3.  Phosphoinositide-Dependent Signaling in Sympathetic Neurons (SCG) (Kruse et al. 2016)
Phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2] is a minor phospholipid in the cytoplasmic leaflet of the plasma membrane. Depletion of PI(4,5)P2 via phospholipase C-mediated hydrolysis leads to a decrease in exocytosis and alters electrical excitability in neurons. Restoration of PI(4,5)P2 is essential for a return to basal neuronal activity. However, the dynamics of phosphoinositide metabolism have not been analyzed in neurons. We studied the dynamics of phosphoinositide metabolism in sympathetic neu- rons upon muscarinic stimulation and used the kinetic information to develop a quantitative description of neuronal phospho- inositide metabolism. The measurements and analysis show a several-fold faster synthesis of PI(4,5)P2 in sympathetic neurons than in an electrically nonexcitable cell line, and provide a framework for future studies of PI(4,5)P2-dependent processes in neurons.
4.  Regulation of KCNQ2/KCNQ3 current by G protein cycling (Suh et al 2004)
Receptor-mediated modulation of KCNQ channels regulates neuronal excitability. This study concerns the kinetics and mechanism of M1 muscarinic receptor-mediated regulation of the cloned neuronal M channel, KCNQ2/KCNQ3 (Kv7.2/Kv7.3). ... observations were successfully described by a kinetic model representing biochemical steps of the signaling cascade using published rate constants where available. The model supports the following sequence of events for this Gq-coupled signaling: A classical G-protein cycle, including competition for nucleotide-free G-protein by all nucleotide forms and an activation step requiring Mg2, followed by G-protein-stimulated phospholipase C and hydrolysis of PIP2, and finally PIP2 dissociation from binding sites for inositol lipid on the channels so that KCNQ current was suppressed. See paper for details and more.

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