Key result
Mice lacking a functional NOS-2 gene had a 32% reduced lesion volume and improved sensorimotor (p=0.011) and cognitive function (p=0.009) compared to wild-type mice after severe cerebral injury.
Why the study?
Does genetic deletion of NOS-2 reduce lesion volume and improve neurological recovery in mice subjected to acute cerebral injury?
Does genetic deletion of NOS-2 reduce lesion volume and improve neurological recovery in mice subjected to acute cerebral injury?
Effect estimate: 32% reduction in lesion volume
p-value: p=0.011, 0.009
Genetic deletion of NOS-2 reduces lesion volume and improves neurological recovery following acute traumatic brain injury in mice, suggesting NOS-2 contributes to neuropathology.
NOS-2 deletion improves murine cerebral injury outcomes; hypothesis-generating for neuroprotection, with human translation untested.
Nitric oxide (NO) synthesized from the inducible isoform of nitric oxide synthase (NOS-2) has been suggested to play both beneficial and deleterious roles in various neuropathologies. To define the role of nitric oxide in traumatic brain injury, we subjected male mice lacking a functional NOS-2 gene (NOS-2-/-) and their wild-type littermates (NOS-2+/+) to mild or severe aseptic cryogenic cerebral injury. Expression of NOS-2 mRNA and protein was observed in NOS-2+/+ animals following injury. Lesion volume (as measured by histology and brain imaging) and neurological outcome (using motor and cognitive behavioral paradigms) were assessed at various times after injury. While magnetic resonance imaging revealed the extent of edema of the 2 genotypes to be similar, histology showed a reduced (32%) lesion volume in severely injured NOS-2-/- compared with NOS-2+/+ mice. In addition, NOS-2-/- mice showed significant improvements in both contralateral sensorimotor deficits (grid test: p = 0.011) and cognitive function (Morris water maze: p = 0.009) after severe injury compared to their wild-type littermates. This indicates that lesion volume is reduced and neurological recovery is improved after acute traumatic injury in mice lacking a functional NOS-2 gene, and strongly suggests that the post-trauma production of NO from this source contributes to neuropathology.
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Jones et al. (2004) studied Traumatic brain injury. Lack of functional NOS-2 gene (NOS-2-/-) vs. Wild-type littermates (NOS-2+/+) was evaluated on Lesion volume and neurological outcome (32% reduction in lesion volume, p=0.011, 0.009). Mice lacking a functional NOS-2 gene had a 32% reduced lesion volume and improved sensorimotor (p=0.011) and cognitive function (p=0.009) compared to wild-type mice after severe cerebral injury.
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