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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.

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Quantification of motoneuronal mitochondria in the spinal cord of intact control, laminectomy and syrinx groups at 1 h, 24 h and 6 weeks after injury. *P < 0.005, versus intact control. †P < 0.05, versus laminectomy at the same time point. ‡P < 0.03, versus intact control.
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fig2: Quantification of motoneuronal mitochondria in the spinal cord of intact control, laminectomy and syrinx groups at 1 h, 24 h and 6 weeks after injury. *P < 0.005, versus intact control. †P < 0.05, versus laminectomy at the same time point. ‡P < 0.03, versus intact control.

Mentions: When evaluating the degree of degeneration, it is not the size and shape, but the number of mitochondria that is important. Quantification of neuronal mitochondria in the grey matter of the spinal cord in intact controls, laminectomy group, and syrinx animals at 1 hour, 1 day, and 6-week time points was shown in Figure 2. There was a similar number of mitochondria in intact controls and laminectomy group at 1 hour time point, the number of mitochondria declined by half in laminectomy group at 24 hours, which then recovered by 24% at 6 weeks. When compared with laminectomy, the number of mitochondria was 2.6- and 1.5-fold lower in syrinx groups at 1 hour and 1 day, respectively, and no mitochondrion was identified in the grey matter surrounding cyst at 6 weeks. Such complete depletion of mitochondria indicates dying neuron.


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

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

Quantification of motoneuronal mitochondria in the spinal cord of intact control, laminectomy and syrinx groups at 1 h, 24 h and 6 weeks after injury. *P < 0.005, versus intact control. †P < 0.05, versus laminectomy at the same time point. ‡P < 0.03, versus intact control.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig2: Quantification of motoneuronal mitochondria in the spinal cord of intact control, laminectomy and syrinx groups at 1 h, 24 h and 6 weeks after injury. *P < 0.005, versus intact control. †P < 0.05, versus laminectomy at the same time point. ‡P < 0.03, versus intact control.
Mentions: When evaluating the degree of degeneration, it is not the size and shape, but the number of mitochondria that is important. Quantification of neuronal mitochondria in the grey matter of the spinal cord in intact controls, laminectomy group, and syrinx animals at 1 hour, 1 day, and 6-week time points was shown in Figure 2. There was a similar number of mitochondria in intact controls and laminectomy group at 1 hour time point, the number of mitochondria declined by half in laminectomy group at 24 hours, which then recovered by 24% at 6 weeks. When compared with laminectomy, the number of mitochondria was 2.6- and 1.5-fold lower in syrinx groups at 1 hour and 1 day, respectively, and no mitochondrion was identified in the grey matter surrounding cyst at 6 weeks. Such complete depletion of mitochondria indicates dying neuron.

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