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Cyclosporin A limits calcium-induced axonal damage following traumatic brain injury
Department of Anatomy, Medical College of Virginia, Virginia Commonwealth University, Richmond, USA.
Department of Anatomy, Medical College of Virginia, Virginia Commonwealth University, Richmond, United States; Department of Neurosurgery, University Medical School of Pécs, Hungary .ORCID iD: 0000-0002-2190-9278
Cephalon, West Chester, PA 19380, USA.
Department of Anatomy, Medical College of Virginia, Virginia Commonwealth University, Richmond, USA.
1999 (English)In: NeuroReport, ISSN 0959-4965, E-ISSN 1473-558X, Vol. 10, no 2, p. 353-358Article in journal (Refereed) Published
Abstract [en]

In traumatic axonal injury, Ca2+ influx across a focally damaged axolemma precipitates local mitochondrial failure, degradation of the subaxolemmal spectrin network and compaction of neurofilaments, which collectively contribute to axonal failure. In previous studies, cyclosporin A pretreatment preserved mitochondrial integrity and attenuated axonal failure following trauma. Here we investigate whether this CsA-linked protection was related to the concomitant blunting of intra-axonal, Ca2+-induced cytoskeletal changes in traumatic axonal injury, assessed with antibodies targeting spectrin proteolysis and neurofilament compaction. CsA pretreatment dramatically reduced Ca2+-induced cytoskeletal damage following injury; CsA-treated rats, compared with vehicle-treated rats, displayed a 70% decrease in immunoreactive/damaged profiles. We suggest that CsA-mediated preservation of mitochondrial integrity enables the restoration of ionic and metabolic homeostasis thereby short-circuiting Ca2+-induced proteolysis in injured axons. 

Place, publisher, year, edition, pages
Lippincott Williams & Wilkins, 1999. Vol. 10, no 2, p. 353-358
National Category
Neurology
Identifiers
URN: urn:nbn:se:oru:diva-113375DOI: 10.1097/00001756-199902050-00026ISI: 000079393000027PubMedID: 10203334Scopus ID: 2-s2.0-0033525008OAI: oai:DiVA.org:oru-113375DiVA, id: diva2:1854465
Funder
NIH (National Institutes of Health), NS20193Available from: 2024-04-25 Created: 2024-04-25 Last updated: 2024-04-25Bibliographically approved

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