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Moderate Posttraumatic Hypothermia Decreases Early Calpain-Mediated Proteolysis and Concomitant Cytoskeletal Compromise in Traumatic Axonal Injury
Department of Anatomy, Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia, USA; Department of Neurosurgery, University Medical School of Pécs, H-7624, Pécs, Hungary.ORCID iD: 0000-0002-2190-9278
Department of Anatomy, Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia, USA; Department of Neurosurgery, Yamaguchi University School of Medicine, 1144 Kogushi, Ube, Yamaguchi, 755, Japan.
Department of Anatomy, Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia, USA.
1999 (English)In: Experimental Neurology, ISSN 0014-4886, E-ISSN 1090-2430, Vol. 159, no 1, p. 319-328Article in journal (Refereed) Published
Abstract [en]

Traumatic brain injury (TBI) in animals and man generates widespread axonal injury characterized by focal axolemmal permeability changes, induction of calpain-mediated proteolysis, and neurofilament side-arm modification associated with neurofilament compaction (NFC) evolving to axonal disconnection. Recent observations have suggested that moderate hypothermia is neuroprotective in several models of TBI. Nevertheless, the pathway by which hypothermia prevents traumatic axonal injury (TAI) is still a matter of debate. The present study was conducted to evaluate the effects of moderate, early posttraumatic hypothermia on calpain-mediated spectrin proteolysis (CMSP), implicated in the pathogenesis of TAI. Using moderate (32 degrees C) hypothermia of 90 min duration without rewarming, the density of CMSP immunoreactive/damaged axons was quantified via LM analysis in vulnerable brain stem fiber tracts of hypothermic and normothermic rats subjected to impact acceleration TBI (90 min postinjury survival). To assess the influence of posthypothermic rewarming, a second group of animals was subjected to 90 min of hypothermia followed by 90 min of rewarming to normothermic levels when CMSP was analyzed to detect if any purported CMSP prevention persisted (180 min postinjury survival). Additionally, to determine if this protection translated into comparable cytoskeletal protection in the same foci showing decreased CMSP, antibodies targeting altered/compacted NF subunits were also employed. Moderate hypothermia applied in the acute postinjury period drastically reduced the number of damaged axons displaying CMSP at both time points and significantly reduced NFC immunoreactivity at 180 min postinjury. These results suggest that the neuroprotective effects of hypothermia in TBI are associated with the inhibition of axonal/cytoskeletal damage. 

Place, publisher, year, edition, pages
Academic Press, 1999. Vol. 159, no 1, p. 319-328
National Category
Neurology
Identifiers
URN: urn:nbn:se:oru:diva-113372DOI: 10.1006/exnr.1999.7139ISI: 000082644700031PubMedID: 10486200Scopus ID: 2-s2.0-2542510324OAI: oai:DiVA.org:oru-113372DiVA, id: diva2:1854445
Conference
2nd Conference of Cellular and Molecular Treatments of Neurological Diseases (CMT), CAMBRIDGE, MASSACHUSETTS, OCT, 1998.
Funder
NIH (National Institutes of Health), NS 20193
Note

This work is supported by Grants NS 20193 and The MartinRodbell Fellowship.

Available from: 2024-04-25 Created: 2024-04-25 Last updated: 2024-04-25Bibliographically approved

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