Journal
JOURNAL OF NEUROSCIENCE
Volume 32, Issue 35, Pages 12028-12037Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.0408-12.2012
Keywords
-
Categories
Funding
- National Institutes of Health [1R01NS057433, 1R01GM069883, T32 NS007381]
- National Multiple Sclerosis Society [CA-1055-A-3]
- Department of Veterans Affairs
- Office of Research and Development
- Biomedical Laboratory of Research and Development
- Laura Fund for Innovation in Multiple Sclerosis Research
- Nancy Davis Center Without Walls
- St. Laurent Foundation of Vancouver
- NIH NINDS [P30NS061800]
Ask authors/readers for more resources
Axonal spheroids occur as part of the pathology of a variety of neurologic diseases. Reactive oxygen species (ROS) trigger formation of spheroids, axonal severing, and Ca2+ overload. The mechanisms by which ROS lead to the spheroid formation at specific axonal sites remain elusive. Here, using adult mouse primary neurons, we investigate the role of Ca2+, its regulating systems, and cytoskeletal changes in formation of axonal spheroids triggered by ROS. The results reveal that dramatically higher axoplasmic Ca2+ levels occur at the sites of axonal spheroids than in the rest of the axon. High focal axoplasmic Ca2+ levels correlate with focal aggregation of the reverse Na+/Ca2+ exchanger 1, voltage-gated N-type Ca2+ channel alpha 1B subunit, and actin at the sites of spheroids in individual axons. This study provides new insights into the mechanism of a spheroid formation at specific sites along axons undergoing oxidative stress and a basis for new neuroprotective strategies.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available