| A detrimental role for nitric oxide synthase-2 in the pathology resulting from acute cerebral injury. | |
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MedLine Citation:
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PMID: 15290896 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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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Authors:
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N C Jones; D Constantin; C L Gibson; M J W Prior; P G Morris; C A Marsden; S Murphy |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Journal of neuropathology and experimental neurology Volume: 63 ISSN: 0022-3069 ISO Abbreviation: J. Neuropathol. Exp. Neurol. Publication Date: 2004 Jul |
Date Detail:
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Created Date: 2004-08-04 Completed Date: 2004-08-26 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 2985192R Medline TA: J Neuropathol Exp Neurol Country: United States |
Other Details:
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Languages: eng Pagination: 708-20 Citation Subset: IM |
Affiliation:
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Institute of Cell Signalling, University of Nottingham, Nottingham, United Kingdom. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Acute Disease Animals Brain Edema / enzymology, genetics, pathology Brain Injuries / enzymology*, genetics, pathology Cerebral Cortex / enzymology*, pathology, physiopathology Cognition Disorders / enzymology, genetics, pathology Magnetic Resonance Imaging Male Maze Learning / physiology Mice Mice, Knockout Movement Disorders / enzymology, genetics, pathology Nerve Degeneration / enzymology*, genetics, pathology Neurons / enzymology, pathology Nitric Oxide / biosynthesis* Nitric Oxide Synthase / biosynthesis, genetics, physiology* Nitric Oxide Synthase Type II RNA, Messenger / metabolism Reaction Time / genetics Recovery of Function / genetics |
| Chemical | |
Reg. No./Substance:
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0/RNA, Messenger; 10102-43-9/Nitric Oxide; EC 1.14.13.39/Nitric Oxide Synthase; EC 1.14.13.39/Nitric Oxide Synthase Type II |
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