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) stained coronal spinal cord sections from laminectomy ((a) and (b)) and syrinx rat model of posttraumatic syringomyelia ((c) and (d)) at 1 hour after syrinx induction procedure.
© Copyright Policy - open-access
Related In: Results  -  Collection


getmorefigures.php?uid=PMC4309244&req=5

fig4: Hematoxylin and eosin (H and E) stained coronal spinal cord sections from laminectomy ((a) and (b)) and syrinx rat model of posttraumatic syringomyelia ((c) and (d)) at 1 hour after syrinx induction procedure.

Mentions: To understand the consequences of ischemia in the context of apoptotic versus necrotic types of neuronal death, we evaluated morphology of apoptosis and necrosis in the spinal cord. At 1 hour time point, there was no cyst formation in the spinal cords of laminectomy or syrinx rats (Figures 4(a) and 4(c)). Ischemic changes were observed in the spinal cords of both laminectomy and syrinx rats but restricted to cells with neuronal morphology, differed in an extent between laminectomy and syrinx rats. Two distinct types of histopathological changes were observed. The first type was characteristic of apoptosis including nuclear and cytoplasmic condensation, nuclear budding, and fragmentation into membrane-bound small bodies (apoptotic bodies) (Figure 4(b)). The second type was characteristic of necrosis including pyknotic nuclei and eosinophilic, structureless cytoplasm (red neurons), or absent nuclear hematoxylin staining (ghost neurons) (Figure 4(d)).


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) stained coronal spinal cord sections from laminectomy ((a) and (b)) and syrinx rat model of posttraumatic syringomyelia ((c) and (d)) at 1 hour after syrinx induction procedure.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig4: Hematoxylin and eosin (H and E) stained coronal spinal cord sections from laminectomy ((a) and (b)) and syrinx rat model of posttraumatic syringomyelia ((c) and (d)) at 1 hour after syrinx induction procedure.
Mentions: To understand the consequences of ischemia in the context of apoptotic versus necrotic types of neuronal death, we evaluated morphology of apoptosis and necrosis in the spinal cord. At 1 hour time point, there was no cyst formation in the spinal cords of laminectomy or syrinx rats (Figures 4(a) and 4(c)). Ischemic changes were observed in the spinal cords of both laminectomy and syrinx rats but restricted to cells with neuronal morphology, differed in an extent between laminectomy and syrinx rats. Two distinct types of histopathological changes were observed. The first type was characteristic of apoptosis including nuclear and cytoplasmic condensation, nuclear budding, and fragmentation into membrane-bound small bodies (apoptotic bodies) (Figure 4(b)). The second type was characteristic of necrosis including pyknotic nuclei and eosinophilic, structureless cytoplasm (red neurons), or absent nuclear hematoxylin staining (ghost neurons) (Figure 4(d)).

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