Key result
Neuronal nitric oxide synthase-deficient mice showed significantly improved hind limb motor function compared to wild-type controls at day 10 (p<0.022) and day 14 (p<0.048) after spinal cord injury.
Why the study?
Does genetic deletion of neuronal NOS or TNF-alpha improve functional recovery after spinal cord injury in mice?
Does genetic deletion of neuronal NOS or TNF-alpha improve functional recovery after spinal cord injury in mice?
p-value: p=<0.022 (day 10), <0.048 (day 14)
Neuronal NOS deficiency, but not TNF-alpha deficiency, improves functional recovery after spinal cord injury in mice, suggesting a detrimental role of NO in secondary damage.
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Neuronal NOS deletion improves motor recovery after SCI in mice; hypothesis-generating for NO-targeted therapies, should not yet change practice.
Farooque et al. (2001) studied Spinal cord injury. Neuronal nitric oxide synthase (NOS) deficiency vs. Wild-type mice was evaluated on Hind limb motor function score (MFS) (p=<0.022 (day 10), <0.048 (day 14)). Neuronal nitric oxide synthase-deficient mice showed significantly improved hind limb motor function compared to wild-type controls at day 10 (p<0.022) and day 14 (p<0.048) after spinal cord injury.
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