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Experimental cauda equina compression induces HSP70 synthesis in dog
D Cízková1, N Lukácová, M Marsala
1Institute of Neurobiology, Slovak Academy of Science, Kosice, Slovak Republic. cizkova@saske.sk
Physiological Research
|June 25, 2005
Summary
Multiple cauda equina constrictions in dogs trigger heat shock protein 70 (HSP70) synthesis in spinal cord neurons and dorsal root ganglion cells. This suggests HSP70 plays a neuroprotective role in cauda equina syndrome.
Area of Science:
- Neuroscience
- Molecular Biology
- Veterinary Medicine
Background:
- Heat shock protein 70 (HSP70) is crucial for cellular stress response.
- Cauda equina syndrome involves compression of nerve roots, leading to neurological deficits.
Purpose of the Study:
- To investigate the expression of HSP70 following multiple cauda equina constrictions (MCEC) in a canine model.
- To understand the role of HSP70 in neuroprotection during nerve root compression.
Main Methods:
- Induction of MCEC in dogs to mimic clinical cauda equina syndrome.
- Assessment of HSP70 immunoreactivity (HSP70-IR) in spinal cord segments and dorsal root ganglia (DRGs).
- Histological analysis of neuronal staining patterns.
Main Results:
- MCEC caused significant HSP70 up-regulation in spinal cord (L7, S1-Co3) and DRGs (L7-S1) within two days.
- HSP70-positive neurons were identified in specific spinal cord regions (ventral horn, lamina X) and DRGs.
- Mild HSP70 upregulation observed in small/medium DRG neurons and satellite cells; no staining in controls.
Conclusions:
- MCEC in dogs induces HSP70 expression in specific spinal cord and DRG neurons.
- HSP70 synthesis suggests an active neuroprotective role in mitigating neuronal damage.
- Findings support HSP70's involvement in maintaining protein integrity and preventing degeneration in this model.