| The pathophysiology of traumatic brain injury (TBI) is often divided into two phases. The acute phase lasts approximately 24 hours after experimental injury and is characterized by neuronal excitation, excess release of neurotransmitters and hypermetabolism. The chronic phase begins 24 hours after injury and lasts weeks to months after injury. The chronic phase is characterized by neuronal depression, impaired release of neurotransmitters and hypometabolism. The present studies investigated the effects of repeated postinjury energy supplementation on Morris water maze performance, circulating blood glucose levels, and expression of cytochrome oxidase in the hippocampus. The results of experiments 1-4 demonstrated that pre-trial glucose treatment produces maximal memory enhancement following TBI. Improvements in spatial memory were not apparent following fructose treatment (experiment 2), post-trial glucose treatment (experiment 3) or 10 days of postinjury glucose treatment terminated before cognitive testing (experiment 4). No significant differences in circulating blood glucose levels were detected in any experiments. Western blot analysis revealed no significant differences in expression of cytochrome oxidase in ipsilateral or contralateral hippocampi. These results suggest that postinjury energy supplementation should be delivered shortly before cognitive testing to detect improvements in cognitive performance. Injury induced decreases in cytochrome oxidase expression appear to resolve by 15 days postinjury. Additional research is needed to clarify specific mechanisms contributing to postinjury glucose induced memory modulation. |
