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Updated: Sep 26, 2026
Spinal Cord Neurons Isolation and Culture from Neonatal Mice
Published on: July 11, 2017
Cyclosporin A reduces delayed motor neuron death after spinal cord ischemia in rabbits
Minato Sato1, Takashi Horinouchi, Masahiro Sakurai
1Department of Anesthesiology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Background:
Spinal cord ischemia has varied etiologies, and in some cases, may develop into paraplegia. This is attributable to the vulnerability of spinal motor neurons to ischemia. We evaluated the potential of the immunosuppressant cyclosporin A for treatment of spinal motor neuron damage caused by ischemia.
Methods:
Twenty-eight rabbits were randomized into four groups of 7 animals each: group A (cyclosporin A not administered), group B (2.5 mg/kg cyclosporin A), group C (25 mg/kg cyclosporin A), and group S (sham-operated). The spinal cord ischemia model was created by a 15-minute occlusion of the aorta just caudal to a renal artery with a balloon catheter. Administration of cyclosporin A began 30 minutes after restoration of blood flow. The spinal cords were removed after 7-day monitoring of neurologic function. Pathology specimens were prepared, and after staining them with hematoxylin-eosin, viable motor neurons in the ventral spinal cord were counted under light microscopy.
Results:
At 7 days after reperfusion, recovery of motor function was seen at varying degrees in groups B and C, whereas all animals in group A continued to exhibit paraplegia. In group C, most of the animals recovered to the baseline level, before creation of the ischemia model. A significant difference in numbers of viable neurons was found in group A (cell count, 10.1 +/- 4.7) and group C (cell count, 22.2 +/- 8.0) (p < 0.05). Higher numbers of viable motor neurons corresponded to a greater recovery of motor function.
Conclusions:
These results suggest that cyclosporin A administration is effective against neuronal damage caused by spinal cord ischemia.
Insights
Cyclosporin A effectively treats spinal cord ischemia and prevents paraplegia by protecting vulnerable motor neurons. This immunosuppressant promotes significant recovery of motor function and increases viable neuron counts in animal models.
Area of Science:
- Neuroscience
- Immunology
- Regenerative Medicine
Background:
- Spinal cord ischemia can lead to paraplegia due to motor neuron vulnerability.
- Investigating therapeutic interventions for spinal cord ischemia is crucial.
Purpose of the Study:
- To evaluate the efficacy of cyclosporin A (CsA) in treating spinal motor neuron damage following ischemia.
- To assess the neuroprotective effects of CsA in a rabbit model of spinal cord ischemia.
Main Methods:
- A rabbit model of spinal cord ischemia was induced via aortic occlusion.
- Animals were randomized into groups receiving different doses of CsA or a sham operation.
- Neurologic function was monitored, and spinal cord pathology was analyzed for viable motor neurons.
Main Results:
- Cyclosporin A administration significantly improved motor function recovery compared to controls.
- Higher doses of CsA (25 mg/kg) led to near-complete motor function recovery.
- A significant increase in viable motor neuron counts was observed in the CsA-treated group.
Conclusions:
- Cyclosporin A demonstrates significant neuroprotective effects against spinal cord ischemia.
- CsA is a promising therapeutic agent for mitigating neuronal damage and functional deficits after spinal cord ischemia.
