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07:47
Analysis of Brain Mitochondria Using Serial Block-Face Scanning Electron Microscopy
Published on: July 9, 2016
Intrinsic differences in brain and spinal cord mitochondria: Implication for therapeutic interventions
Patrick G Sullivan1, Alexander G Rabchevsky, Jeffery N Keller
1Spinal Cord and Brain Injury Research Center, University of Kentucky, Lexington, Kentucky 40536, USA. patsull@uky.edu
The Journal of Comparative Neurology
|June 3, 2004
Summary
Spinal cord neurons exhibit higher oxidative stress and impaired mitochondrial function compared to brain neurons. These intrinsic differences may explain why treatments effective for brain injury fail in spinal cord injury.
Area of Science:
- Neuroscience
- Mitochondrial Physiology
- Central Nervous System (CNS) Injury
Background:
- Central nervous system (CNS) regions exhibit differential responses to injury.
- Cyclosporine A effectively reduces brain injury but is ineffective for spinal cord injury.
- Intrinsic differences in neuronal physiology may underlie this therapeutic disparity.
Purpose of the Study:
- To investigate the physiological differences in mitochondria between the neocortex and spinal cord.
- To identify factors contributing to the differential response to injury in CNS regions.
- To explore potential therapeutic targets for spinal cord injury.
Main Methods:
- In situ measurements of mitochondrial physiology, including O(2)(-) production, lipid peroxidation, and mitochondrial DNA oxidation.
- Real-time PCR to analyze mitochondrial transcripts.
- Assessment of Complex I enzyme activity and respiration in isolated mitochondria.
- Determination of the calcium-induced mitochondrial permeability transition threshold.
Main Results:
- Spinal cord neurons showed significantly higher levels of oxidative stress markers (O(2)(-) production, lipid peroxidation, mtDNA oxidation) compared to neocortical neurons.
- Spinal cord mitochondria exhibited altered mitochondrial transcripts, decreased Complex I activity, and reduced respiration.
- The threshold for calcium-induced mitochondrial permeability transition was lower in spinal cord mitochondria and influenced by lipid peroxidation.
Conclusions:
- Intrinsic differences in mitochondrial physiology, particularly heightened oxidative stress and impaired function, exist between spinal cord and neocortical neurons.
- These disparities may explain the differential efficacy of therapeutic interventions like cyclosporine A.
- Targeting these intrinsic differences offers a potential strategy for ameliorating neuronal damage in spinal cord injury and related neuropathologies like amyotrophic lateral sclerosis.
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