Mitochondrial Permeability Transition in the CNS - Composition, Regulation, and Pathophysiological Relevance

Tadeusz Wieloch; Gustav Mattiasson; Magnus Hansson; Eskil Elmer

doi:10.1007/978-0-387-30411-3_25

Mitochondrial Permeability Transition in the CNS - Composition, Regulation, and Pathophysiological Relevance

Tadeusz Wieloch, Gustav Mattiasson, Magnus Hansson, Eskil Elmer

Sektion IV

Forskningsoutput: Kapitel i bok/rapport/Conference proceeding › Kapitel samlingsverk › Forskning

Sammanfattning

Mitochondrial permeability transition (MPT) is induced in isolated brain mitochondria by calcium and oxidants and is inhibited by adenine nucleotides. When induced, MPT is associated with equilibration of solutes of <1500 Da across the inner mitochondrial membrane. A persistent induction of MPT depolarizes the inner membrane and causes cessation of ATP synthesis, swelling of the matrix, and bursting of the mitochondrial membranes. The rupture of the membranes releases calcium stored in the mitochondrial matrix and apoptogenic factors from the intermembrane space, leading to cell death. MPT has been implicated in acute brain injury and neurodegenerative disease since inhibitors of MPT such as cyclosporin A (CsA) are brain protective. Whether MPT has a physiological role is unclear, but MPT may be important in calcium homeostasis under conditions of excessive neuronal activity.

Originalspråk	engelska
Titel på värdpublikation	Handbook of Neurochemistry and Molecular Neurobiology - Brain Energetics. Integration of Molecular and Cellular Processes
Redaktörer	Abel Lajtha, Gary E Gibson, Gerry A Dienel
Förlag	Springer
Sidor	667-702
ISBN (tryckt)	978-0-387-30366-6
DOI	https://doi.org/10.1007/978-0-387-30411-3_25
Status	Published - 2007

Bibliografisk information

The information about affiliations in this record was updated in December 2015.
The record was previously connected to the following departments: Laboratory for Experimental Brain Research (013041000)

Ämnesklassifikation (UKÄ)

Neurologi

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10.1007/978-0-387-30411-3_25

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Wieloch, T., Mattiasson, G., Hansson, M., & Elmer, E. (2007). Mitochondrial Permeability Transition in the CNS - Composition, Regulation, and Pathophysiological Relevance. I A. Lajtha, G. E. Gibson, & G. A. Dienel (Red.), Handbook of Neurochemistry and Molecular Neurobiology - Brain Energetics. Integration of Molecular and Cellular Processes (s. 667-702). Springer. https://doi.org/10.1007/978-0-387-30411-3_25

Wieloch, Tadeusz ; Mattiasson, Gustav ; Hansson, Magnus et al. / Mitochondrial Permeability Transition in the CNS - Composition, Regulation, and Pathophysiological Relevance. Handbook of Neurochemistry and Molecular Neurobiology - Brain Energetics. Integration of Molecular and Cellular Processes. redaktör / Abel Lajtha ; Gary E Gibson ; Gerry A Dienel. Springer, 2007. s. 667-702

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abstract = "Mitochondrial permeability transition (MPT) is induced in isolated brain mitochondria by calcium and oxidants and is inhibited by adenine nucleotides. When induced, MPT is associated with equilibration of solutes of <1500 Da across the inner mitochondrial membrane. A persistent induction of MPT depolarizes the inner membrane and causes cessation of ATP synthesis, swelling of the matrix, and bursting of the mitochondrial membranes. The rupture of the membranes releases calcium stored in the mitochondrial matrix and apoptogenic factors from the intermembrane space, leading to cell death. MPT has been implicated in acute brain injury and neurodegenerative disease since inhibitors of MPT such as cyclosporin A (CsA) are brain protective. Whether MPT has a physiological role is unclear, but MPT may be important in calcium homeostasis under conditions of excessive neuronal activity.",

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Wieloch, T , Mattiasson, G , Hansson, M & Elmer, E 2007, Mitochondrial Permeability Transition in the CNS - Composition, Regulation, and Pathophysiological Relevance. i A Lajtha, GE Gibson & GA Dienel (red), Handbook of Neurochemistry and Molecular Neurobiology - Brain Energetics. Integration of Molecular and Cellular Processes. Springer, s. 667-702. https://doi.org/10.1007/978-0-387-30411-3_25

Mitochondrial Permeability Transition in the CNS - Composition, Regulation, and Pathophysiological Relevance. / Wieloch, Tadeusz ; Mattiasson, Gustav ; Hansson, Magnus et al.

Handbook of Neurochemistry and Molecular Neurobiology - Brain Energetics. Integration of Molecular and Cellular Processes. red. / Abel Lajtha; Gary E Gibson; Gerry A Dienel. Springer, 2007. s. 667-702.

Forskningsoutput: Kapitel i bok/rapport/Conference proceeding › Kapitel samlingsverk › Forskning

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N1 - The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Laboratory for Experimental Brain Research (013041000)

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AB - Mitochondrial permeability transition (MPT) is induced in isolated brain mitochondria by calcium and oxidants and is inhibited by adenine nucleotides. When induced, MPT is associated with equilibration of solutes of <1500 Da across the inner mitochondrial membrane. A persistent induction of MPT depolarizes the inner membrane and causes cessation of ATP synthesis, swelling of the matrix, and bursting of the mitochondrial membranes. The rupture of the membranes releases calcium stored in the mitochondrial matrix and apoptogenic factors from the intermembrane space, leading to cell death. MPT has been implicated in acute brain injury and neurodegenerative disease since inhibitors of MPT such as cyclosporin A (CsA) are brain protective. Whether MPT has a physiological role is unclear, but MPT may be important in calcium homeostasis under conditions of excessive neuronal activity.

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Wieloch T , Mattiasson G , Hansson M , Elmer E. Mitochondrial Permeability Transition in the CNS - Composition, Regulation, and Pathophysiological Relevance. I Lajtha A, Gibson GE, Dienel GA, redaktörer, Handbook of Neurochemistry and Molecular Neurobiology - Brain Energetics. Integration of Molecular and Cellular Processes. Springer. 2007. s. 667-702 doi: 10.1007/978-0-387-30411-3_25

Mitochondrial Permeability Transition in the CNS - Composition, Regulation, and Pathophysiological Relevance

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