Multiscale model of dynamic neuromodulation integrating neuropeptide-induced signaling pathway activity with membrane electrophysiology.

@article{Makadia2015MultiscaleMO,
  title={Multiscale model of dynamic neuromodulation integrating neuropeptide-induced signaling pathway activity with membrane electrophysiology.},
  author={Hirenkumar K. Makadia and Warren D. Anderson and Dirk Fey and Thomas Sauter and James S. Schwaber and Rajanikanth Vadigepalli},
  journal={Biophysical journal},
  year={2015},
  volume={108 1},
  pages={211-23}
}
We developed a multiscale model to bridge neuropeptide receptor-activated signaling pathway activity with membrane electrophysiology. Typically, the neuromodulation of biochemical signaling and biophysics have been investigated separately in modeling studies. We studied the effects of Angiotensin II (AngII) on neuronal excitability changes mediated by signaling dynamics and downstream phosphorylation of ion channels. Experiments have shown that AngII binding to the AngII receptor type-1 elicits… CONTINUE READING

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We examined the relative contributions of signaling kinases protein kinase C and Ca(2+)/Calmodulin - dependent protein kinase II to AngII - mediated excitability changes by simulating activity blockade individually and in combination .
We found that protein kinase C selectively controlled firing rate adaptation whereas Ca(2+)/Calmodulin - dependent protein kinase II induced a delayed effect on the firing rate increase .
We examined the relative contributions of signaling kinases protein kinase C and Ca(2+)/Calmodulin - dependent protein kinase II to AngII - mediated excitability changes by simulating activity blockade individually and in combination .
We found that protein kinase C selectively controlled firing rate adaptation whereas Ca(2+)/Calmodulin - dependent protein kinase II induced a delayed effect on the firing rate increase .
We examined the relative contributions of signaling kinases protein kinase C and Ca(2+)/Calmodulin - dependent protein kinase II to AngII - mediated excitability changes by simulating activity blockade individually and in combination .
We found that protein kinase C selectively controlled firing rate adaptation whereas Ca(2+)/Calmodulin - dependent protein kinase II induced a delayed effect on the firing rate increase .
We examined the relative contributions of signaling kinases protein kinase C and Ca(2+)/Calmodulin - dependent protein kinase II to AngII - mediated excitability changes by simulating activity blockade individually and in combination .
We found that protein kinase C selectively controlled firing rate adaptation whereas Ca(2+)/Calmodulin - dependent protein kinase II induced a delayed effect on the firing rate increase .
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