Pro-Apoptotic Changes in Brain Mitochondria After Toxic Exposure
Abstract
Mitochondria normally function to provide sources of energy for vital cellular functions. However, under stressful conditions these organelles may trigger events that lead eventually to cell death. Thus, mitochondria have been implicated as major contributors to neuronal death in a variety of neurodegenerative disorders. In this report we provide evidence that certain mitochondrial toxins cause selective cell death in hippocampal subfield CA1 that has previously been shown to be selectively vulnerable to hypoxia/ischemia. We have also measured changes in mitochondrial membrane potential following toxin exposure. Little mitochondrial depolarization was observed at times when electrophysiology was compromised. Finally, we provide preliminary evidence of redistribution of cytochrome c following toxin exposure. This redistribution was seen primarily in hippocampal subfield CA1 and in the dentate gyrus. Activation of Caspase-3 was only observed in the dentate gyrus, suggesting that activation of this pro-apoptotic factor may not be responsible for cell death in the CA1 subfield.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jul 01, 2001
- Accession Number
- ADA397717
Entities
People
- Thomas J. Sick
Organizations
- University of Miami