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Feedback Regulation of Calcium Concentration

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Calcium is an essential signaling molecule required for various cellular functions. Calcium pumps and ion channels on cell and organellar membranes, such as those on the endoplasmic reticulum (ER), regulate calcium concentrations inside the cell. They remain closed, keeping the cytosolic calcium levels low at a resting state.
Various transmembrane receptors, such as G protein-coupled receptors (GPCRs), elicit a response to extracellular signals by increasing cytosolic calcium. Activated GPCRs...

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Imaging Local Ca2+ Signals in Cultured Mammalian Cells

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Published on: March 3, 2015

Multi-scale data-driven modeling and observation of calcium puffs.

Ghanim Ullah¹, Ian Parker, Don-On Daniel Mak

¹Theoretical Biology and Biophysics, Los Alamos National Laboratory, NM, United States.

|June 12, 2012

Summary

Calcium puffs terminate due to self-inhibition of inositol 1,4,5-trisphosphate receptors (IP(3)Rs), not endoplasmic reticulum (ER) calcium depletion. This study models puff dynamics using single-channel data to reveal termination mechanisms.

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Functional Calcium Imaging in Developing Cortical Networks

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Published on: October 22, 2011

Area of Science:

Cellular Biology
Biophysics
Biochemistry

Background:

Elementary calcium (Ca2+) release events, like blips and puffs, are fundamental to cellular signaling.
The precise mechanisms governing calcium puff termination remain poorly understood.

Purpose of the Study:

To investigate the termination mechanism of calcium puffs using a data-driven approach.
To elucidate the role of inositol 1,4,5-trisphosphate receptors (IP(3)Rs) in puff dynamics.

Main Methods:

Developed a computational model of IP(3)R kinetics based on single-channel patch clamp data.
Simulated calcium puff events to analyze their spatiotemporal dynamics.
Utilized a data-driven approach to identify key factors in puff termination.

Main Results:

The model successfully reproduced observed blip and puff dynamics.
Simulations indicate that puffs terminate due to IP(3)R self-inhibition through a kinetic loop.
Endoplasmic reticulum (ER) Ca2+ depletion was ruled out as a cause for puff termination.
Estimated single IP(3)R current and peak Ca2+ concentration near the pore.

Conclusions:

Calcium puff termination is primarily driven by IP(3)R self-inhibition.
The study provides a mechanistic understanding of puff termination, distinct from ER Ca2+ depletion.
The data-driven model offers insights into IP(3)R gating and Ca2+ signaling.