Limits...
The roads to mitochondrial dysfunction in a rat model of posttraumatic syringomyelia.

Hu Z, Tu J - Biomed Res Int (2015)

Bottom Line: 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.We found an 86 ± 11% reduction of local blood flow at C8 where a cyst formed at 6 weeks after syrinx induction procedure (P < 0.05), and no difference in blood flow rate between the laminectomy and intact controls.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurosurgery, Beijing Shijitan Hospital, Capital Medical University, Beijing 100038, China.

ABSTRACT
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 86 ± 11% reduction of local blood flow at C8 where a cyst formed at 6 weeks after syrinx induction procedure (P < 0.05), 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.

Show MeSH

Related in: MedlinePlus

Hematoxylin and eosin (H and E) staining of coronal spinal cord sections from laminectomy ((a)–(d)) and syrinx rat model of posttraumatic syringomyelia ((e)–(h)) at 6 weeks after syrinx induction procedure.
© Copyright Policy - open-access
Related In: Results  -  Collection


getmorefigures.php?uid=PMC4309244&req=5

fig6: Hematoxylin and eosin (H and E) staining of coronal spinal cord sections from laminectomy ((a)–(d)) and syrinx rat model of posttraumatic syringomyelia ((e)–(h)) at 6 weeks after syrinx induction procedure.

Mentions: At 6-week time point, there was no cyst formation in the spinal cords of laminectomy animals (Figures 6(a)–6(d)) although spongy with numerous vacuolations (Figures 6(b) and 6(c)), ischemic neuronal change and ghost neurons (Figure 6(d)), and lymphocyte infiltration could be seen in the grey matter. In contrast to laminectomy (Figure 6(a)), cysts were observed as cystic spaces within the cord (Figure 6(e)), sometimes containing cellular debris and a loose trabecular meshwork (Figure 6(f)) in the syrinx rats. Syringes extended from the grey matter to white matter (Figure 6(e)). The syrinx margin was defined as an interface between normal tissue and cystic spaces (Figure 6(g)). In the normal tissue, there were a small percentage of motoneurons undergoing ischemic cell change, and even ghost neurons were seen (Figure 6(h)).


The roads to mitochondrial dysfunction in a rat model of posttraumatic syringomyelia.

Hu Z, Tu J - Biomed Res Int (2015)

Hematoxylin and eosin (H and E) staining of coronal spinal cord sections from laminectomy ((a)–(d)) and syrinx rat model of posttraumatic syringomyelia ((e)–(h)) at 6 weeks after syrinx induction procedure.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4309244&req=5

fig6: Hematoxylin and eosin (H and E) staining of coronal spinal cord sections from laminectomy ((a)–(d)) and syrinx rat model of posttraumatic syringomyelia ((e)–(h)) at 6 weeks after syrinx induction procedure.
Mentions: At 6-week time point, there was no cyst formation in the spinal cords of laminectomy animals (Figures 6(a)–6(d)) although spongy with numerous vacuolations (Figures 6(b) and 6(c)), ischemic neuronal change and ghost neurons (Figure 6(d)), and lymphocyte infiltration could be seen in the grey matter. In contrast to laminectomy (Figure 6(a)), cysts were observed as cystic spaces within the cord (Figure 6(e)), sometimes containing cellular debris and a loose trabecular meshwork (Figure 6(f)) in the syrinx rats. Syringes extended from the grey matter to white matter (Figure 6(e)). The syrinx margin was defined as an interface between normal tissue and cystic spaces (Figure 6(g)). In the normal tissue, there were a small percentage of motoneurons undergoing ischemic cell change, and even ghost neurons were seen (Figure 6(h)).

Bottom Line: 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.We found an 86 ± 11% reduction of local blood flow at C8 where a cyst formed at 6 weeks after syrinx induction procedure (P < 0.05), and no difference in blood flow rate between the laminectomy and intact controls.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurosurgery, Beijing Shijitan Hospital, Capital Medical University, Beijing 100038, China.

ABSTRACT
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 86 ± 11% reduction of local blood flow at C8 where a cyst formed at 6 weeks after syrinx induction procedure (P < 0.05), 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.

Show MeSH
Related in: MedlinePlus