Modelling Cross Talk in the Spatiotemporal System Dynamics of Calcium, IP3 and Nitric Oxide in Neuron Cells
The bioenergetic system of calcium ([Ca 2+ ]), inositol 1, 4, 5-trisphophate (IP 3 ) and nitric oxide (NO) regulate the diverse mechanisms in neurons. The dysregulation in any or all of the calcium, IP 3 and nitric oxide dynamics may cause neurotoxicity and cell death. Few studies are noted in the l...
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| Veröffentlicht in: | Cell biochemistry and biophysics 2024-06, Vol.82 (2), p.787-803 |
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| description | The bioenergetic system of calcium ([Ca
2+
]), inositol 1, 4, 5-trisphophate (IP
3
) and nitric oxide (NO) regulate the diverse mechanisms in neurons. The dysregulation in any or all of the calcium, IP
3
and nitric oxide dynamics may cause neurotoxicity and cell death. Few studies are noted in the literature on the interactions of two systems like [Ca
2+
] with IP
3
and [Ca
2+
] with nitric oxide in neuron cells, which gives limited insights into regulatory and dysregulatory processes in neuron cells. But, no study is available on the cross talk in dynamics of three systems [Ca
2+
], IP
3
and NO in neurons. Thus, the cross talk in the system dynamics of [Ca
2+
], IP
3
and NO regulation processes in neurons have been studied using mathematical model. The two-way feedback process between [Ca
2+
] and IP
3
and two-way feedback process between [Ca
2+
] and NO through cyclic guanosine monophosphate (cGMP) with plasmalemmal [Ca
2+
]-ATPase (PMCA) have been incorporated in the proposed model. This coupling handles the indirect two-way feedback process between IP
3
and nitric oxide in neuronal cells automatically. The numerical outcomes were acquired by employing the finite element method (FEM) with the Crank-Nicholson scheme (CNS). The present model incorporating the sodium-calcium exchanger (NCX) and voltage-gated calcium channel (VGCC) provides novel insights into the various regulatory and dysregulatory processes due to buffer, IP
3
-receptor, ryanodine receptor, cGMP kinetics through PMCA channel, etc. and their impacts on the interactive spatiotemporal system dynamics of [Ca
2+
], IP
3
and NO in neurons. It is concluded that the behavior of different crucial mechanisms is quite different for interactions of two systems of [Ca
2+
] and NO and the interactions of three systems of [Ca
2+
], IP
3
and nitric oxide in neuronal cell due to mutual regulatory adjustments. The association of several neurological disorders with the alterations in calcium, IP
3
and NO has been explored in neurons. |
| doi_str_mv | 10.1007/s12013-024-01229-5 |
| format | Article |
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2+
]), inositol 1, 4, 5-trisphophate (IP
3
) and nitric oxide (NO) regulate the diverse mechanisms in neurons. The dysregulation in any or all of the calcium, IP
3
and nitric oxide dynamics may cause neurotoxicity and cell death. Few studies are noted in the literature on the interactions of two systems like [Ca
2+
] with IP
3
and [Ca
2+
] with nitric oxide in neuron cells, which gives limited insights into regulatory and dysregulatory processes in neuron cells. But, no study is available on the cross talk in dynamics of three systems [Ca
2+
], IP
3
and NO in neurons. Thus, the cross talk in the system dynamics of [Ca
2+
], IP
3
and NO regulation processes in neurons have been studied using mathematical model. The two-way feedback process between [Ca
2+
] and IP
3
and two-way feedback process between [Ca
2+
] and NO through cyclic guanosine monophosphate (cGMP) with plasmalemmal [Ca
2+
]-ATPase (PMCA) have been incorporated in the proposed model. This coupling handles the indirect two-way feedback process between IP
3
and nitric oxide in neuronal cells automatically. The numerical outcomes were acquired by employing the finite element method (FEM) with the Crank-Nicholson scheme (CNS). The present model incorporating the sodium-calcium exchanger (NCX) and voltage-gated calcium channel (VGCC) provides novel insights into the various regulatory and dysregulatory processes due to buffer, IP
3
-receptor, ryanodine receptor, cGMP kinetics through PMCA channel, etc. and their impacts on the interactive spatiotemporal system dynamics of [Ca
2+
], IP
3
and NO in neurons. It is concluded that the behavior of different crucial mechanisms is quite different for interactions of two systems of [Ca
2+
] and NO and the interactions of three systems of [Ca
2+
], IP
3
and nitric oxide in neuronal cell due to mutual regulatory adjustments. The association of several neurological disorders with the alterations in calcium, IP
3
and NO has been explored in neurons.</description><identifier>ISSN: 1085-9195</identifier><identifier>ISSN: 1559-0283</identifier><identifier>EISSN: 1559-0283</identifier><identifier>DOI: 10.1007/s12013-024-01229-5</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Biochemistry ; Biological and Medical Physics ; Biomedical and Life Sciences ; Biophysics ; Biotechnology ; Ca2+-transporting ATPase ; Calcium buffering ; Calcium channels ; Calcium channels (voltage-gated) ; Calcium ions ; Calcium oxide ; Calcium signalling ; Cell Biology ; Cell death ; Channel gating ; Crosstalk ; Cyclic GMP ; Feedback ; Finite element method ; Inositol trisphosphate ; Inositols ; Interactive systems ; Kinetics ; Life Sciences ; Mathematical models ; Na+/Ca2+ exchanger ; Neurological diseases ; Neurons ; Neurotoxicity ; Nitric oxide ; Original Paper ; Pharmacology/Toxicology ; Receptors ; Sodium channels (voltage-gated) ; System dynamics</subject><ispartof>Cell biochemistry and biophysics, 2024-06, Vol.82 (2), p.787-803</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2024. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c352t-a9939339ea06aa53176086f9441de87e50c27dd03914fa89c7b7524a2759e38f3</citedby><cites>FETCH-LOGICAL-c352t-a9939339ea06aa53176086f9441de87e50c27dd03914fa89c7b7524a2759e38f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12013-024-01229-5$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12013-024-01229-5$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27923,27924,41487,42556,51318</link.rule.ids></links><search><creatorcontrib>Pawar, Anand</creatorcontrib><creatorcontrib>Pardasani, Kamal Raj</creatorcontrib><title>Modelling Cross Talk in the Spatiotemporal System Dynamics of Calcium, IP3 and Nitric Oxide in Neuron Cells</title><title>Cell biochemistry and biophysics</title><addtitle>Cell Biochem Biophys</addtitle><description>The bioenergetic system of calcium ([Ca
2+
]), inositol 1, 4, 5-trisphophate (IP
3
) and nitric oxide (NO) regulate the diverse mechanisms in neurons. The dysregulation in any or all of the calcium, IP
3
and nitric oxide dynamics may cause neurotoxicity and cell death. Few studies are noted in the literature on the interactions of two systems like [Ca
2+
] with IP
3
and [Ca
2+
] with nitric oxide in neuron cells, which gives limited insights into regulatory and dysregulatory processes in neuron cells. But, no study is available on the cross talk in dynamics of three systems [Ca
2+
], IP
3
and NO in neurons. Thus, the cross talk in the system dynamics of [Ca
2+
], IP
3
and NO regulation processes in neurons have been studied using mathematical model. The two-way feedback process between [Ca
2+
] and IP
3
and two-way feedback process between [Ca
2+
] and NO through cyclic guanosine monophosphate (cGMP) with plasmalemmal [Ca
2+
]-ATPase (PMCA) have been incorporated in the proposed model. This coupling handles the indirect two-way feedback process between IP
3
and nitric oxide in neuronal cells automatically. The numerical outcomes were acquired by employing the finite element method (FEM) with the Crank-Nicholson scheme (CNS). The present model incorporating the sodium-calcium exchanger (NCX) and voltage-gated calcium channel (VGCC) provides novel insights into the various regulatory and dysregulatory processes due to buffer, IP
3
-receptor, ryanodine receptor, cGMP kinetics through PMCA channel, etc. and their impacts on the interactive spatiotemporal system dynamics of [Ca
2+
], IP
3
and NO in neurons. It is concluded that the behavior of different crucial mechanisms is quite different for interactions of two systems of [Ca
2+
] and NO and the interactions of three systems of [Ca
2+
], IP
3
and nitric oxide in neuronal cell due to mutual regulatory adjustments. The association of several neurological disorders with the alterations in calcium, IP
3
and NO has been explored in neurons.</description><subject>Biochemistry</subject><subject>Biological and Medical Physics</subject><subject>Biomedical and Life Sciences</subject><subject>Biophysics</subject><subject>Biotechnology</subject><subject>Ca2+-transporting ATPase</subject><subject>Calcium buffering</subject><subject>Calcium channels</subject><subject>Calcium channels (voltage-gated)</subject><subject>Calcium ions</subject><subject>Calcium oxide</subject><subject>Calcium signalling</subject><subject>Cell Biology</subject><subject>Cell death</subject><subject>Channel gating</subject><subject>Crosstalk</subject><subject>Cyclic GMP</subject><subject>Feedback</subject><subject>Finite element method</subject><subject>Inositol trisphosphate</subject><subject>Inositols</subject><subject>Interactive systems</subject><subject>Kinetics</subject><subject>Life Sciences</subject><subject>Mathematical models</subject><subject>Na+/Ca2+ exchanger</subject><subject>Neurological diseases</subject><subject>Neurons</subject><subject>Neurotoxicity</subject><subject>Nitric oxide</subject><subject>Original Paper</subject><subject>Pharmacology/Toxicology</subject><subject>Receptors</subject><subject>Sodium channels (voltage-gated)</subject><subject>System dynamics</subject><issn>1085-9195</issn><issn>1559-0283</issn><issn>1559-0283</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><recordid>eNp9kF1LwzAUhosoOKd_wKuAN15YzUfTJJdSvwZzEzavQ0zTma1tZtKC-_dmVhC88CqH8LzvOTxJco7gNYKQ3QSEISIpxFkKEcYipQfJCFEq4hcnh3GGnKYCCXqcnISwhhBjmGWjZPPsSlPXtl2BwrsQwFLVG2Bb0L0bsNiqzrrONFvnVQ0WuxBncLdrVWN1AK4Chaq17ZsrMHkhQLUlmNnOWw3mn7Y0-5qZ6b1rQRF3hNPkqFJ1MGc_7zh5fbhfFk_pdP44KW6nqSYUd6kSgghChFEwV4oSxHLI80pkGSoNZ4ZCjVlZQiJQVikuNHtjFGcKMyoM4RUZJ5dD79a7j96ETjY26HiBao3rg8QCc04xE1lEL_6ga9f7Nl4nCRQ55ZwwHik8UHqvyJtKbr1tlN9JBOXevxz8y-hffvuXNIbIEAoRblfG_1b_k_oCS3KGIw</recordid><startdate>20240601</startdate><enddate>20240601</enddate><creator>Pawar, Anand</creator><creator>Pardasani, Kamal Raj</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20240601</creationdate><title>Modelling Cross Talk in the Spatiotemporal System Dynamics of Calcium, IP3 and Nitric Oxide in Neuron Cells</title><author>Pawar, Anand ; Pardasani, Kamal Raj</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c352t-a9939339ea06aa53176086f9441de87e50c27dd03914fa89c7b7524a2759e38f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Biochemistry</topic><topic>Biological and Medical Physics</topic><topic>Biomedical and Life Sciences</topic><topic>Biophysics</topic><topic>Biotechnology</topic><topic>Ca2+-transporting ATPase</topic><topic>Calcium buffering</topic><topic>Calcium channels</topic><topic>Calcium channels (voltage-gated)</topic><topic>Calcium ions</topic><topic>Calcium oxide</topic><topic>Calcium signalling</topic><topic>Cell Biology</topic><topic>Cell death</topic><topic>Channel gating</topic><topic>Crosstalk</topic><topic>Cyclic GMP</topic><topic>Feedback</topic><topic>Finite element method</topic><topic>Inositol trisphosphate</topic><topic>Inositols</topic><topic>Interactive systems</topic><topic>Kinetics</topic><topic>Life Sciences</topic><topic>Mathematical models</topic><topic>Na+/Ca2+ exchanger</topic><topic>Neurological diseases</topic><topic>Neurons</topic><topic>Neurotoxicity</topic><topic>Nitric oxide</topic><topic>Original Paper</topic><topic>Pharmacology/Toxicology</topic><topic>Receptors</topic><topic>Sodium channels (voltage-gated)</topic><topic>System dynamics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pawar, Anand</creatorcontrib><creatorcontrib>Pardasani, Kamal Raj</creatorcontrib><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Cell biochemistry and biophysics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pawar, Anand</au><au>Pardasani, Kamal Raj</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Modelling Cross Talk in the Spatiotemporal System Dynamics of Calcium, IP3 and Nitric Oxide in Neuron Cells</atitle><jtitle>Cell biochemistry and biophysics</jtitle><stitle>Cell Biochem Biophys</stitle><date>2024-06-01</date><risdate>2024</risdate><volume>82</volume><issue>2</issue><spage>787</spage><epage>803</epage><pages>787-803</pages><issn>1085-9195</issn><issn>1559-0283</issn><eissn>1559-0283</eissn><abstract>The bioenergetic system of calcium ([Ca
2+
]), inositol 1, 4, 5-trisphophate (IP
3
) and nitric oxide (NO) regulate the diverse mechanisms in neurons. The dysregulation in any or all of the calcium, IP
3
and nitric oxide dynamics may cause neurotoxicity and cell death. Few studies are noted in the literature on the interactions of two systems like [Ca
2+
] with IP
3
and [Ca
2+
] with nitric oxide in neuron cells, which gives limited insights into regulatory and dysregulatory processes in neuron cells. But, no study is available on the cross talk in dynamics of three systems [Ca
2+
], IP
3
and NO in neurons. Thus, the cross talk in the system dynamics of [Ca
2+
], IP
3
and NO regulation processes in neurons have been studied using mathematical model. The two-way feedback process between [Ca
2+
] and IP
3
and two-way feedback process between [Ca
2+
] and NO through cyclic guanosine monophosphate (cGMP) with plasmalemmal [Ca
2+
]-ATPase (PMCA) have been incorporated in the proposed model. This coupling handles the indirect two-way feedback process between IP
3
and nitric oxide in neuronal cells automatically. The numerical outcomes were acquired by employing the finite element method (FEM) with the Crank-Nicholson scheme (CNS). The present model incorporating the sodium-calcium exchanger (NCX) and voltage-gated calcium channel (VGCC) provides novel insights into the various regulatory and dysregulatory processes due to buffer, IP
3
-receptor, ryanodine receptor, cGMP kinetics through PMCA channel, etc. and their impacts on the interactive spatiotemporal system dynamics of [Ca
2+
], IP
3
and NO in neurons. It is concluded that the behavior of different crucial mechanisms is quite different for interactions of two systems of [Ca
2+
] and NO and the interactions of three systems of [Ca
2+
], IP
3
and nitric oxide in neuronal cell due to mutual regulatory adjustments. The association of several neurological disorders with the alterations in calcium, IP
3
and NO has been explored in neurons.</abstract><cop>New York</cop><pub>Springer US</pub><doi>10.1007/s12013-024-01229-5</doi><tpages>17</tpages></addata></record> |
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| subjects | Biochemistry Biological and Medical Physics Biomedical and Life Sciences Biophysics Biotechnology Ca2+-transporting ATPase Calcium buffering Calcium channels Calcium channels (voltage-gated) Calcium ions Calcium oxide Calcium signalling Cell Biology Cell death Channel gating Crosstalk Cyclic GMP Feedback Finite element method Inositol trisphosphate Inositols Interactive systems Kinetics Life Sciences Mathematical models Na+/Ca2+ exchanger Neurological diseases Neurons Neurotoxicity Nitric oxide Original Paper Pharmacology/Toxicology Receptors Sodium channels (voltage-gated) System dynamics |
| title | Modelling Cross Talk in the Spatiotemporal System Dynamics of Calcium, IP3 and Nitric Oxide in Neuron Cells |
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