Spinal cord mitochondria display lower calcium retention capacity compared with brain mitochondria without inherent differences in sensitivity to cyclophilin D inhibition
(2007) In Journal of Neurochemistry 103(5). p.2066-2076- Abstract
- The mitochondrial permeability transition (mPT) is a potential pathogenic mechanism in neurodegeneration. Varying sensitivity to calcium-induced mPT has been demonstrated for regions within the CNS possibly correlating with vulnerability following insults. The spinal cord is selectively vulnerable in e.g. amyotrophic lateral sclerosis and increased mPT sensitivity of mitochondria derived from the spinal cord has previously been demonstrated. In this study, we introduce whole-body hypothermia prior to removal of CNS tissue to minimize the effects of differential tissue extraction prior to isolation of spinal cord and cortical brain mitochondria. Spinal cord mitochondria were able to retain considerably less calcium when administered as... (More)
- The mitochondrial permeability transition (mPT) is a potential pathogenic mechanism in neurodegeneration. Varying sensitivity to calcium-induced mPT has been demonstrated for regions within the CNS possibly correlating with vulnerability following insults. The spinal cord is selectively vulnerable in e.g. amyotrophic lateral sclerosis and increased mPT sensitivity of mitochondria derived from the spinal cord has previously been demonstrated. In this study, we introduce whole-body hypothermia prior to removal of CNS tissue to minimize the effects of differential tissue extraction prior to isolation of spinal cord and cortical brain mitochondria. Spinal cord mitochondria were able to retain considerably less calcium when administered as continuous infusion, which was not related to a general increased sensitivity of the mPT to calcium, its desensitization to calcium by the cyclophilin D inhibitor cyclosporin-A, or to differences in respiratory parameters. Spinal cord mitochondria maintained a higher concentration of extramitochondrial calcium during infusion than brain mitochondria possibly related to an increased set-point concentration for calcium uptake. A hampered transport and retention capacity of calcium may translate into an increased susceptibility of the spinal cord to neurodegenerative processes involving calcium-mediated damage. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/971877
- author
- Morota, Saori ; Hansson, Magnus LU ; Ishii, Nagao ; Kudo, Yoshihisa ; Elmer, Eskil LU and Uchino, Hiroyuki
- organization
- publishing date
- 2007
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- cord injury, spinal, neurodegeneration, necrosis, ischemia, apoptosis, cell death
- in
- Journal of Neurochemistry
- volume
- 103
- issue
- 5
- pages
- 2066 - 2076
- publisher
- Wiley-Blackwell
- external identifiers
-
- wos:000250985200034
- scopus:36248984867
- pmid:17868326
- ISSN
- 1471-4159
- DOI
- 10.1111/j.1471-4159.2007.04912.x
- language
- English
- LU publication?
- yes
- additional info
- 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)
- id
- d09ef558-3c4a-4655-8baa-253221ab8bd2 (old id 971877)
- date added to LUP
- 2016-04-01 16:15:18
- date last changed
- 2024-01-11 04:34:34
@article{d09ef558-3c4a-4655-8baa-253221ab8bd2, abstract = {{The mitochondrial permeability transition (mPT) is a potential pathogenic mechanism in neurodegeneration. Varying sensitivity to calcium-induced mPT has been demonstrated for regions within the CNS possibly correlating with vulnerability following insults. The spinal cord is selectively vulnerable in e.g. amyotrophic lateral sclerosis and increased mPT sensitivity of mitochondria derived from the spinal cord has previously been demonstrated. In this study, we introduce whole-body hypothermia prior to removal of CNS tissue to minimize the effects of differential tissue extraction prior to isolation of spinal cord and cortical brain mitochondria. Spinal cord mitochondria were able to retain considerably less calcium when administered as continuous infusion, which was not related to a general increased sensitivity of the mPT to calcium, its desensitization to calcium by the cyclophilin D inhibitor cyclosporin-A, or to differences in respiratory parameters. Spinal cord mitochondria maintained a higher concentration of extramitochondrial calcium during infusion than brain mitochondria possibly related to an increased set-point concentration for calcium uptake. A hampered transport and retention capacity of calcium may translate into an increased susceptibility of the spinal cord to neurodegenerative processes involving calcium-mediated damage.}}, author = {{Morota, Saori and Hansson, Magnus and Ishii, Nagao and Kudo, Yoshihisa and Elmer, Eskil and Uchino, Hiroyuki}}, issn = {{1471-4159}}, keywords = {{cord injury; spinal; neurodegeneration; necrosis; ischemia; apoptosis; cell death}}, language = {{eng}}, number = {{5}}, pages = {{2066--2076}}, publisher = {{Wiley-Blackwell}}, series = {{Journal of Neurochemistry}}, title = {{Spinal cord mitochondria display lower calcium retention capacity compared with brain mitochondria without inherent differences in sensitivity to cyclophilin D inhibition}}, url = {{http://dx.doi.org/10.1111/j.1471-4159.2007.04912.x}}, doi = {{10.1111/j.1471-4159.2007.04912.x}}, volume = {{103}}, year = {{2007}}, }