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BioMed Research International
Volume 2015, Article ID 831490, 15 pages
Research Article

The Roads to Mitochondrial Dysfunction in a Rat Model of Posttraumatic Syringomyelia

1Department of Neurosurgery, Beijing Shijitan Hospital, Capital Medical University, Beijing 100038, China
2Prince of Wales Clinical School, The University of New South Wales, Sydney, NSW 2052, Australia

Received 12 May 2014; Accepted 13 October 2014

Academic Editor: Ancha Baranova

Copyright © 2015 Zhiqiang Hu and Jian Tu. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The pathophysiology of posttraumatic syringomyelia is incompletely understood. We examined whether local ischemia occurs after spinal cord injury. If so, whether it causes neuronal mitochondrial dysfunction and depletion, and subsequent energy metabolism impairment results in cell starvation of energy and even cell death, contributing to the enlargement of the cavity. Local blood flow was measured in a rat model of posttraumatic syringomyelia that had received injections of quisqualic acid and kaolin. We found an % reduction of local blood flow at C8 where a cyst formed at 6 weeks after syrinx induction procedure , and no difference in blood flow rate between the laminectomy and intact controls. Electron microscopy confirmed irreversible neuronal mitochondrion depletion surrounding the cyst, but recoverable mitochondrial loses in laminectomy rats. Profound energy loss quantified in the spinal cord of syrinx animals, and less ATP and ADP decline observed in laminectomy rats. Our findings demonstrate that an excitotoxic injury induces local ischemia in the spinal cord and results in neuronal mitochondrial depletion, and profound ATP loss, contributing to syrinx enlargement. Ischemia did not occur following laminectomy induced trauma in which mitochondrial loss and decline in ATP were reversible. This confirms excitotoxic injury contributing to the pathology of posttraumatic syringomyelia.