Termination of Ca²+ release for clustered IP₃R channels.

In many cell types, release of calcium ions is controlled by inositol 1,4,5-trisphosphate (IP₃) receptor channels. Elevations in Ca²⁺ concentration after intracellular release through IP₃ receptors (IP₃R) can either propagate in the form of waves spreading through the entire cell or produce spatiall...

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Autores principales:	Sten Rüdiger, Peter Jung, Jian-Wei Shuai
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/b28bbc083887478bb8b0bf6f220a2bd6
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spelling	oai:doaj.org-article:b28bbc083887478bb8b0bf6f220a2bd62021-11-18T05:51:18ZTermination of Ca²+ release for clustered IP₃R channels.1553-734X1553-735810.1371/journal.pcbi.1002485https://doaj.org/article/b28bbc083887478bb8b0bf6f220a2bd62012-05-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22693433/?tool=EBIhttps://doaj.org/toc/1553-734Xhttps://doaj.org/toc/1553-7358In many cell types, release of calcium ions is controlled by inositol 1,4,5-trisphosphate (IP₃) receptor channels. Elevations in Ca²⁺ concentration after intracellular release through IP₃ receptors (IP₃R) can either propagate in the form of waves spreading through the entire cell or produce spatially localized puffs. The appearance of waves and puffs is thought to implicate random initial openings of one or a few channels and subsequent activation of neighboring channels because of an "autocatalytic" feedback. It is much less clear, however, what determines the further time course of release, particularly since the lifetime is very different for waves (several seconds) and puffs (around 100 ms). Here we study the lifetime of Ca²⁺ signals and their dependence on residual Ca²⁺ microdomains. Our general idea is that Ca²⁺ microdomains are dynamical and mediate the effect of other physiological processes. Specifically, we focus on the mechanism by which Ca²⁺ binding proteins (buffers) alter the lifetime of Ca²⁺ signals. We use stochastic simulations of channel gating coupled to a coarse-grained description for the Ca²⁺ concentration. To describe the Ca²⁺ concentration in a phenomenological way, we here introduce a differential equation, which reflects the buffer characteristics by a few effective parameters. This non-stationary model for microdomains gives deep insight into the dynamical differences between puffs and waves. It provides a novel explanation for the different lifetimes of puffs and waves and suggests that puffs are terminated by Ca²⁺ inhibition while IP₃ unbinding is responsible for termination of waves. Thus our analysis hints at an additional role of IP3 and shows how cells can make use of the full complexity in IP₃R gating behavior to achieve different signals.Sten RüdigerPeter JungJian-Wei ShuaiPublic Library of Science (PLoS)articleBiology (General)QH301-705.5ENPLoS Computational Biology, Vol 8, Iss 5, p e1002485 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Biology (General) QH301-705.5
spellingShingle	Biology (General) QH301-705.5 Sten Rüdiger Peter Jung Jian-Wei Shuai Termination of Ca²+ release for clustered IP₃R channels.
description	In many cell types, release of calcium ions is controlled by inositol 1,4,5-trisphosphate (IP₃) receptor channels. Elevations in Ca²⁺ concentration after intracellular release through IP₃ receptors (IP₃R) can either propagate in the form of waves spreading through the entire cell or produce spatially localized puffs. The appearance of waves and puffs is thought to implicate random initial openings of one or a few channels and subsequent activation of neighboring channels because of an "autocatalytic" feedback. It is much less clear, however, what determines the further time course of release, particularly since the lifetime is very different for waves (several seconds) and puffs (around 100 ms). Here we study the lifetime of Ca²⁺ signals and their dependence on residual Ca²⁺ microdomains. Our general idea is that Ca²⁺ microdomains are dynamical and mediate the effect of other physiological processes. Specifically, we focus on the mechanism by which Ca²⁺ binding proteins (buffers) alter the lifetime of Ca²⁺ signals. We use stochastic simulations of channel gating coupled to a coarse-grained description for the Ca²⁺ concentration. To describe the Ca²⁺ concentration in a phenomenological way, we here introduce a differential equation, which reflects the buffer characteristics by a few effective parameters. This non-stationary model for microdomains gives deep insight into the dynamical differences between puffs and waves. It provides a novel explanation for the different lifetimes of puffs and waves and suggests that puffs are terminated by Ca²⁺ inhibition while IP₃ unbinding is responsible for termination of waves. Thus our analysis hints at an additional role of IP3 and shows how cells can make use of the full complexity in IP₃R gating behavior to achieve different signals.
format	article
author	Sten Rüdiger Peter Jung Jian-Wei Shuai
author_facet	Sten Rüdiger Peter Jung Jian-Wei Shuai
author_sort	Sten Rüdiger
title	Termination of Ca²+ release for clustered IP₃R channels.
title_short	Termination of Ca²+ release for clustered IP₃R channels.
title_full	Termination of Ca²+ release for clustered IP₃R channels.
title_fullStr	Termination of Ca²+ release for clustered IP₃R channels.
title_full_unstemmed	Termination of Ca²+ release for clustered IP₃R channels.
title_sort	termination of ca²+ release for clustered ip₃r channels.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/b28bbc083887478bb8b0bf6f220a2bd6
work_keys_str_mv	AT stenrudiger terminationofca2releaseforclusteredip3rchannels AT peterjung terminationofca2releaseforclusteredip3rchannels AT jianweishuai terminationofca2releaseforclusteredip3rchannels
_version_	1718424749708673024

Termination of Ca²+ release for clustered IP₃R channels.

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