Reduction of the Neurological Deficit in Mice with Traumatic Brain Injury by Nitric Oxide Synthase Inhibitors

Mésenge, Christian; Verrecchia, C.; Allix, Monique; Boulu, R; Plotkine, Michel

doi:10.1089/neu.1996.13.11

Cited by 79 publications

(27 citation statements)

References 19 publications

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“…Both penicillamine (Hall et al, 1999) and tempol (Beit-Yannai et al, 1996) have been reported to improve neurological recovery in rodent TBI models. Moreover, administration of the NOS inhibitors nitro-arginine methyl ester and 7-nitroindazole have been shown to improve neurological recovery in head-injured mice (Mesenge et al, 1996) together with a reduction in brain 3NT levels (Mesenge et al, 1998).…”

Section: Sources Of Peroxynitritementioning

confidence: 99%

Temporal relationship of peroxynitrite-induced oxidative damage, calpain-mediated cytoskeletal degradation and neurodegeneration after traumatic brain injury

Deng

Thompson

Gao

et al. 2007

Experimental Neurology

133

171

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We assessed the temporal and spatial characteristics of PN-induced oxidative damage and its relationship to calpain-mediated cytoskeletal degradation and neurodegeneration in a severe unilateral controlled cortical impact (CCI) traumatic brain injury (TBI) model. Quantitative temporal time-course studies were performed to measure two oxidative damage markers: 3-nitrotyrosine (3NT) and 4-hydroxynonenal (4HNE) at 30 min, 1, 3, 6, 12, 24, 48, 72 hrs, 7 days after injury in ipsilateral cortex of young adult male CF-1 mice. Secondly, the time course of Ca ++ -activated, calpain-mediated proteolysis was also analyzed using quantitative western-blot measurement of breakdown products of the cytoskeletal protein α-spectrin. Finally, the time course of neurodegeneration was examined using de Olmos silver staining. Both oxidative damage markers increased in cortical tissue immediately after injury (30 min) and elevated for the first 3-6 hrs before returning to baseline. In the immunostaining study, the PN-selective marker, 3NT, and the lipid peroxidation marker, 4HNE, were intense and overlapping in the injured cortical tissue. α-Spectrin breakdown products, which was used as biomarker for calpain-mediated cytoskeletal degradation, were also increased after injury, but the time course lagged behind the peak of oxidative damage and did not reach its maximum until 24 hrs post-injury. In turn, cytoskeletal degradation preceded the peak of neurodegeneration which occurred at 48 hrs post-injury. These studies have led us to the hypothesis that PN-mediated oxidative damage is an early event that contributes to a compromise of Ca ++ homeostatic mechanisms which causes a massive Ca ++ overload and calpain activation which is a final common pathway that results in post-traumatic neurodegeneration.

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Section: Sources Of Peroxynitritementioning

confidence: 99%

Temporal relationship of peroxynitrite-induced oxidative damage, calpain-mediated cytoskeletal degradation and neurodegeneration after traumatic brain injury

Deng

Thompson

Gao

et al. 2007

Experimental Neurology

133

171

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“…Nitric oxide (NO) has been suggested to play a role in damage, recovery, or both after brain injury Mesenge et al, 1996;Holscher, 1997). Three different systems are reportedly involved in NO synthesis.…”

Section: Nitric Oxidementioning

confidence: 99%

A Review and Rationale for the Use of Genetically Engineered Animals in the Study of Traumatic Brain Injury

Longhi

Saatman

Raghupathi

et al. 2001

J Cereb Blood Flow Metab

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Summary:The mechanisms underlying secondary cell death after traumatic brain injury (TBI) are poorly understood. Animal models of TBI recapitulate many clinical and pathologic aspects of human head injury, and the development of genetically engineered animals has offered the opportunity to investigate the specific molecular and cellular mechanisms associated with cell dysfunction and death after TBI, allowing for the evaluation of specific cause-effect relations and mechanistic hypotheses. This article represents a compendium of the current literature using genetically engineered mice in studies designed to better understand the posttraumatic inflammatory response, the mechanisms underlying DNA damage, repair, and cell death, and the link between TBI and neurodegenerative diseases.

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“…However, the exact role of elevated NO after injury remains controversial. Inhibition of NO synthase has been shown to increase mortality22 and also reduce neurological deficits23 after experimental contusion in rats. It is possible that different isoforms of NO synthase may have different roles.…”

Section: Introductionmentioning

confidence: 99%

Cerebrovascular reactivity assessed by transcranial Doppler ultrasound in sport-related concussion: a systematic review

et al. 2014

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Reduction of the Neurological Deficit in Mice with Traumatic Brain Injury by Nitric Oxide Synthase Inhibitors

Cited by 79 publications

References 19 publications

Temporal relationship of peroxynitrite-induced oxidative damage, calpain-mediated cytoskeletal degradation and neurodegeneration after traumatic brain injury

Temporal relationship of peroxynitrite-induced oxidative damage, calpain-mediated cytoskeletal degradation and neurodegeneration after traumatic brain injury

A Review and Rationale for the Use of Genetically Engineered Animals in the Study of Traumatic Brain Injury

Cerebrovascular reactivity assessed by transcranial Doppler ultrasound in sport-related concussion: a systematic review

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