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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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Related in: MedlinePlus

Quantification of adenine nucleotide at C8 level of the spinal cord of intact control, laminectomy and syrinx groups at 1 h, 24 h, and 6 weeks after injury. Data expressed as mean ± SE from 4–21 separate experiments. (a) ATP concentration. *P < 0.05, versus laminectomy and syrinx animals at the same time point. †P < 0.05, versus corresponding groups at 1 h and 6 weeks. ‡P < 0.05, versus intact and laminectomy at the same time point. (b) ADP concentration. *P < 0.05, versus laminectomy and syrinx animals at the same time point. †P < 0.05, versus laminectomy at the same time point, and syrinx animals at 1 h and 6 weeks after injury. ‡P < 0.05, versus intact, laminectomy at 1 and 24 h. ΔP < 0.05, versus intact and laminectomy at the same time point and syrinx group at 24 h. (c) AMP concentration. *P < 0.05, versus intact and syrinx at the same time point. †P < 0.05, versus intact and laminectomy at the same time point. ‡P < 0.05, versus intact, laminectomy at the same time point, and syrinx at 1 h.
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fig3: Quantification of adenine nucleotide at C8 level of the spinal cord of intact control, laminectomy and syrinx groups at 1 h, 24 h, and 6 weeks after injury. Data expressed as mean ± SE from 4–21 separate experiments. (a) ATP concentration. *P < 0.05, versus laminectomy and syrinx animals at the same time point. †P < 0.05, versus corresponding groups at 1 h and 6 weeks. ‡P < 0.05, versus intact and laminectomy at the same time point. (b) ADP concentration. *P < 0.05, versus laminectomy and syrinx animals at the same time point. †P < 0.05, versus laminectomy at the same time point, and syrinx animals at 1 h and 6 weeks after injury. ‡P < 0.05, versus intact, laminectomy at 1 and 24 h. ΔP < 0.05, versus intact and laminectomy at the same time point and syrinx group at 24 h. (c) AMP concentration. *P < 0.05, versus intact and syrinx at the same time point. †P < 0.05, versus intact and laminectomy at the same time point. ‡P < 0.05, versus intact, laminectomy at the same time point, and syrinx at 1 h.

Mentions: There is a correlation between the number of mitochondria and the energy synthesis of the cell. Adenine nucleotide levels in the spinal cord at C8 were summarized in Figure 3. Comparing with the levels of ATP, and ADP in normal controls, energy levels in the laminectomy group declined at 1 hour after injury and partially recovered at later time points. In contrast, such an initial energy reduction did not recover in the spinal cords with syringes (Figures 3(a) and 3(b)). Increasing levels of AMP with time were recorded in syrinx group (Figure 3(c)).


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

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

Quantification of adenine nucleotide at C8 level of the spinal cord of intact control, laminectomy and syrinx groups at 1 h, 24 h, and 6 weeks after injury. Data expressed as mean ± SE from 4–21 separate experiments. (a) ATP concentration. *P < 0.05, versus laminectomy and syrinx animals at the same time point. †P < 0.05, versus corresponding groups at 1 h and 6 weeks. ‡P < 0.05, versus intact and laminectomy at the same time point. (b) ADP concentration. *P < 0.05, versus laminectomy and syrinx animals at the same time point. †P < 0.05, versus laminectomy at the same time point, and syrinx animals at 1 h and 6 weeks after injury. ‡P < 0.05, versus intact, laminectomy at 1 and 24 h. ΔP < 0.05, versus intact and laminectomy at the same time point and syrinx group at 24 h. (c) AMP concentration. *P < 0.05, versus intact and syrinx at the same time point. †P < 0.05, versus intact and laminectomy at the same time point. ‡P < 0.05, versus intact, laminectomy at the same time point, and syrinx at 1 h.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig3: Quantification of adenine nucleotide at C8 level of the spinal cord of intact control, laminectomy and syrinx groups at 1 h, 24 h, and 6 weeks after injury. Data expressed as mean ± SE from 4–21 separate experiments. (a) ATP concentration. *P < 0.05, versus laminectomy and syrinx animals at the same time point. †P < 0.05, versus corresponding groups at 1 h and 6 weeks. ‡P < 0.05, versus intact and laminectomy at the same time point. (b) ADP concentration. *P < 0.05, versus laminectomy and syrinx animals at the same time point. †P < 0.05, versus laminectomy at the same time point, and syrinx animals at 1 h and 6 weeks after injury. ‡P < 0.05, versus intact, laminectomy at 1 and 24 h. ΔP < 0.05, versus intact and laminectomy at the same time point and syrinx group at 24 h. (c) AMP concentration. *P < 0.05, versus intact and syrinx at the same time point. †P < 0.05, versus intact and laminectomy at the same time point. ‡P < 0.05, versus intact, laminectomy at the same time point, and syrinx at 1 h.
Mentions: There is a correlation between the number of mitochondria and the energy synthesis of the cell. Adenine nucleotide levels in the spinal cord at C8 were summarized in Figure 3. Comparing with the levels of ATP, and ADP in normal controls, energy levels in the laminectomy group declined at 1 hour after injury and partially recovered at later time points. In contrast, such an initial energy reduction did not recover in the spinal cords with syringes (Figures 3(a) and 3(b)). Increasing levels of AMP with time were recorded in syrinx group (Figure 3(c)).

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