Methylprednisolone Treatment Does Not Influence Axonal Regeneration or Degeneration Following Optic Nerve Injury in the Adult Rat

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Title Journal of Neuro-Ophthalmology, March 2004, Volume 24, Issue 1
Date 2004-03
Language eng
Format application/pdf
Type Text
Publication Type Journal Article
Collection Neuro-Ophthalmology Virtual Education Library: Journal of Neuro-Ophthalmology Archives: https://novel.utah.edu/jno/
Publisher Lippincott, Williams & Wilkins
Holding Institution Spencer S. Eccles Health Sciences Library, University of Utah
Rights Management © North American Neuro-Ophthalmology Society
ARK ark:/87278/s6p87j0r
Setname ehsl_novel_jno
ID 225388
Reference URL https://collections.lib.utah.edu/ark:/87278/s6p87j0r

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Title Methylprednisolone Treatment Does Not Influence Axonal Regeneration or Degeneration Following Optic Nerve Injury in the Adult Rat
Creator Ohlsson, M; Westerlund, U; Langmoen, IA; Svensson, M
Affiliation Department of Clinical Neuroscience, Section of Neurosurgery, Karolinska Institute and Hospital, Stockholm, Sweden. marcus.ohlsson@ks.se
Abstract BACKGROUND: Methylprednisolone (MP) is often used to treat optic nerve injury. However, its effects in experimental crush injury have not been extensively evaluated. METHODS: Adult Sprague-Dawley rats were subjected to a standardized optic nerve crush injury. Animals were treated either with 30 mg/kg MP intravenous bolus followed by subcutaneous injections every 6 hours for 48 hours, or with a drug vehicle alone. RESULTS: The injury resulted in a partial loss of neuronal nuclei-labeled retinal neurons and a corresponding degeneration of axons distal to the injury. EDI-labeled macrophages accumulated at the site of lesion, phagocyting FJ-labeled axonal debris. Regenerative fibers expressing growth associated protein-43 were seen proximal to the lesion, but did not traverse the glial scar. Analysis of optic nerve function using visual evoked potentials showed typical signals in intact animals, which were abolished after injury in MP-treated and untreated animals. CONCLUSIONS: We did not detect any effects of MP on retinal cell survival, macrophage activity at the site of injury, axonal degeneration/regeneration, or visual function. These experimental results provide a physiologic underpinning for the lack of efficacy demonstrated in a large trial of MP treatment of clinical optic nerve injury.
Subject Animals; Axons/drug effects; Axons/ultrastructure; Ectodysplasins; Evoked Potentials, Visual/drug effects; Female; Fluorescent Dyes; GAP-43 Protein/metabolism; Macrophages/metabolism; Macrophages/pathology; Membrane Proteins/metabolism; Methylprednisolone/pharmacology; Nerve Crush; Nerve Degeneration/etiology; Nerve Degeneration/physiopathology; Nerve Regeneration/drug effects; Neuroprotective Agents/pharmacology; Optic Nerve Injuries/complications; Optic Nerve Injuries/metabolism; Optic Nerve Injuries/pathology; Optic Nerve Injuries/physiopathology; Organic Chemicals; Rats; Rats, Sprague-Dawley; Retinal Ganglion Cells/pathology; Wounds, Nonpenetrating/physiopathology
OCR Text Show
Format application/pdf
Publication Type Journal Article
Collection Neuro-Ophthalmology Virtual Education Library: Journal of Neuro-Ophthalmology Archives: https://novel.utah.edu/jno/
Publisher Lippincott, Williams & Wilkins
Holding Institution Spencer S. Eccles Health Sciences Library, University of Utah
Rights Management © North American Neuro-Ophthalmology Society
Setname ehsl_novel_jno
ID 225372
Reference URL https://collections.lib.utah.edu/ark:/87278/s6p87j0r/225372
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