AI Article Synopsis
- Different regions of the central nervous system (CNS) react differently to injuries, with cyclosporine A being effective for brain injuries but not for spinal cord injuries.
- Research shows that spinal cord neurons have higher oxidative stress indicators than neocortical neurons, reflecting worse mitochondrial health.
- These findings suggest that the unique mitochondrial characteristics of spinal cord neurons may be key to developing treatments for spinal cord injuries and conditions like amyotrophic lateral sclerosis.
Article Abstract
It is well known that regions of the CNS differentially respond to insults. After brain injury, cyclosporine A reduces damage but is ineffective following spinal cord injury. We address this disparity by assessing several parameters of mitochondrial physiology in the normal neocortex and spinal cord. In situ measurements of O(2) (-.) production, lipid peroxidation, and mitochondrial DNA oxidation revealed significantly higher levels in spinal cord vs. neocortical neurons. Real-time PCR demonstrated differences in mitochondrial transcripts coupled with decreases in complex I enzyme activity and respiration in spinal cord mitochondria. The threshold for calcium-induced mitochondrial permeability transition was substantially reduced in spinal cord vs. neocortex and modulated by lipid peroxidation. These intrinsic differences may provide a pivotal target for strategies to ameliorate neuronal damage following injury, and this imbalance in oxidative stress may contribute to the susceptibility of spinal cord motor neurons in neuropathologies such as amyotrophic lateral sclerosis.
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| http://dx.doi.org/10.1002/cne.20130 | DOI Listing |
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