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

Wieloch, Tadeusz LU ; Mattiasson, Gustav LU ; Hansson, Magnus LU and Elmer, Eskil LU (2007) In Handbook of Neurochemistry and Molecular Neurobiology - Brain Energetics. Integration of Molecular and Cellular Processes p.667-702
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.... (More)
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. (Less)
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author
organization
publishing date
type
Chapter in Book/Report/Conference proceeding
publication status
published
subject
in
Handbook of Neurochemistry and Molecular Neurobiology - Brain Energetics. Integration of Molecular and Cellular Processes
editor
Lajtha, Abel; Gibson, Gary E and Dienel, Gerry A
pages
667 - 702
publisher
Springer
external identifiers
  • Scopus:84900975500
ISBN
978-0-387-30366-6
DOI
10.1007/978-0-387-30411-3_25
language
English
LU publication?
yes
id
391475ba-7c3c-4d17-973b-6f57699213b4 (old id 1141445)
date added to LUP
2008-08-25 13:01:42
date last changed
2016-10-30 04:40:14
@misc{391475ba-7c3c-4d17-973b-6f57699213b4,
  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 &lt;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.},
  author       = {Wieloch, Tadeusz and Mattiasson, Gustav and Hansson, Magnus and Elmer, Eskil},
  editor       = {Lajtha, Abel and Gibson, Gary E and Dienel, Gerry A},
  isbn         = {978-0-387-30366-6},
  language     = {eng},
  pages        = {667--702},
  publisher    = {ARRAY(0x99c77c8)},
  series       = {Handbook of Neurochemistry and Molecular Neurobiology - Brain Energetics. Integration of Molecular and Cellular Processes},
  title        = {Mitochondrial Permeability Transition in the CNS - Composition, Regulation, and Pathophysiological Relevance},
  url          = {http://dx.doi.org/10.1007/978-0-387-30411-3_25},
  year         = {2007},
}