Format

Send to

Choose Destination
PLoS One. 2014 May 21;9(5):e97750. doi: 10.1371/journal.pone.0097750. eCollection 2014.

Repetitive long-term hyperbaric oxygen treatment (HBOT) administered after experimental traumatic brain injury in rats induces significant remyelination and a recovery of sensorimotor function.

Author information

1
Research Unit for Experimental Neurotraumatology, Medical University of Graz, Graz, Austria.
2
Department of Neurosurgery, Medical University of Graz, Graz, Austria.
3
Clinical Division of General Neurology, Medical University of Graz, Graz, Austria.
4
Core Facility Microscopy, Centre for Medical Research, Medical University of Graz, Graz, Austria.
5
Division of Thoracic and Hyperbaric Surgery, Department of Surgery, Medical University of Graz, Graz, Austria.
6
Department of Neurosurgery, University of Cologne, Cologne, Germany; Institute of Neurophysiology, University of Cologne, Cologne, Germany.

Abstract

Cells in the central nervous system rely almost exclusively on aerobic metabolism. Oxygen deprivation, such as injury-associated ischemia, results in detrimental apoptotic and necrotic cell loss. There is evidence that repetitive hyperbaric oxygen therapy (HBOT) improves outcomes in traumatic brain-injured patients. However, there are no experimental studies investigating the mechanism of repetitive long-term HBOT treatment-associated protective effects. We have therefore analysed the effect of long-term repetitive HBOT treatment on brain trauma-associated cerebral modulations using the lateral fluid percussion model for rats. Trauma-associated neurological impairment regressed significantly in the group of HBO-treated animals within three weeks post trauma. Evaluation of somatosensory-evoked potentials indicated a possible remyelination of neurons in the injured hemisphere following HBOT. This presumption was confirmed by a pronounced increase in myelin basic protein isoforms, PLP expression as well as an increase in myelin following three weeks of repetitive HBO treatment. Our results indicate that protective long-term HBOT effects following brain injury is mediated by a pronounced remyelination in the ipsilateral injured cortex as substantiated by the associated recovery of sensorimotor function.

PMID:
24848795
PMCID:
PMC4029808
DOI:
10.1371/journal.pone.0097750
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Public Library of Science Icon for PubMed Central
Loading ...
Support Center