Journal of neurotrauma
-
Journal of neurotrauma · Jun 2007
Time course of early metabolic changes following diffuse traumatic brain injury in rats as detected by (1)H NMR spectroscopy.
Experimental models of traumatic brain injury (TBI) provide a useful tool for understanding the cerebral metabolic changes induced by this pathological condition. Here, we report on the time course of changes in cerebral metabolites after TBI and its correlation with early brain morphological changes using a combination of high-resolution proton magnetic resonance spectroscopy ((1)H MRS) and magnetic resonance imaging (MRI). Adult male Sprague-Dawley rats were subjected to closed head impact and examined by MRI at 1, 9, 24, 48, and and 72 h after the injury. ⋯ The third one involved creatine-phosphocreatine, N-acetylaspartate, and myo-inositol, with concentrations peaking 48 h after the injury. A multivariate stepwise discriminant analysis revealed that the combination of the organic osmolytes taurine and myo-inositol allowed optimal discrimination among the different time groups. Our findings suggest that the profile of some specific brain molecules that play a role as organic osmolytes can be used to follow-up the progression of the early diffuse brain edema response induced by TBI.
-
Journal of neurotrauma · Jun 2007
Calpain inhibitor MDL-28170 reduces the functional and structural deterioration of corpus callosum following fluid percussion injury.
It is known that calpain activation is involved in human traumatic brain injury (TBI) and that calpain inhibition can have neuroprotective effects on both gray matter and white matter injury of TBI models. However, the role of calpain activation in the corpus callosum remains unclear and requires elucidation given its potential clinical relevance. We evaluated the neuroprotective effects of calpain inhibitor MDL-28170 on corpus callosum function and structural destruction using a fluid percussion injury (FPI) model. ⋯ Our data indicated that calpain inhibitor MDL-28170 is an effective neuroprotectant for axonal injury in corpus callosum following FPI with a therapeutic time window up to 4 hours. Although delayed treatment (2 or 4 h post FPI) was effective in protecting the axonal structure, the axons saved may not be as functional as normal fibers. Multiple drug administrations may be necessary for achieving a persisting effectiveness of this compound.