ArticleMolecular and cellular biochemistry2013
Mitochondrial respiratory chain and creatine kinase activities following trauma brain injury in brain of mice preconditioned with N-methyl-D-aspartate.
Article in Molecular and cellular biochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.
- A Systematic Review of Closed Head Injury Models of Mild Traumatic Brain Injury in Mice and Rats.Journal of neurotrauma · 2019Pooled it
- Polydatin prevents the induction of secondary brain injury after traumatic brain injury by protecting neuronal mitochondria.Neural regeneration research · 2019Article
- SIRT1 plays a neuroprotective role in traumatic brain injury in rats via inhibiting the p38 MAPK pathway.Acta pharmacologica Sinica · 2017Article
- What's New in Traumatic Brain Injury: Update on Tracking, Monitoring and Treatment.International journal of molecular sciences · 2015Review
- Neuroprotection induced by NMDA preconditioning as a strategy to understand brain tolerance mechanism.Neural regeneration research · 2015Article
- Brain high-energy phosphates and creatine kinase synthesis rate under graded isoflurane anesthesia: An in vivo (31) P magnetization transfer study at 11.7 tesla.Magnetic resonance in medicine · 2015Article
- The Role of NMDA Receptors in the Development of Brain Resistance through Pre- and Postconditioning.Aging and disease · 2014Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Traumatic brain injury (TBI) induces glutamatergic excitotoxicity through N-methyl-D-aspartate (NMDA) receptors, affecting the integrity of the mitochondrial membrane. Studies have pointed to mitochondria as the master organelle in the preconditioning-triggered endogenous neuroprotective response. The present study is aimed at understanding energy metabolism in the brains of mice after preconditioning with NMDA and TBI. For this purpose, male albino CF-1 mice were pre-treated with NMDA (75 mg/kg) and subjected to brain trauma. Mitochondrial respiratory chain and creatine kinase activities were assessed at 6 or 24 h after trauma. The mice preconditioned and subjected to TBI exhibited augmented activities of complexes II and IV in the cerebral cortex and/or cerebellum. Creatine kinase activity was also augmented in the cerebral cortex after 24 h. We suggest that even though NMDA preconditioning and TBI have similar effects on enzyme activities, each manage their response via opposite mechanisms because the protective effects of preconditioning are unambiguous. In conclusion, NMDA preconditioning induces protection via an increase of enzymes in the mitochondria.
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