The overall goal of the UCLA Brain Injury Research (BIRC) Program is to understand the neurobiology of human traumatic brain injury (TBI). Our basic science efforts have described much of the neurochemical and metabolic cascade that is initiated by TBI. Out off these efforts, we have described how TBI increases the extracellular concentration of potassium. This injury- induced ionic flux increases the demand for energy to drive sodium/potassium pumps. The demand for this energy is primarily satisfied from the selective activation of glycolysis. Utilizing [14 C]deoxy-D-glucose autoradiography in experimental animals, we have been able to detect the extend of this injury-induced hyperglycolysis thereby obtaining an "image of the insult".

Incorporating both conventional and state-of-the-art metabolic imaging studies, we have been successful in documenting the injury-induced hyperglycolysis occurs following humain TBI. From our preliminary findingd, the mechanisms behind the increase in glucose metabolism and its effect on neurophysiology are identical to what we have described in our animal models of TBI. This project will determine the regional distribution of hyperglycolysis following human TBI utilizing positron emission tomography (PET). It will also address the ideology and consequences of hyperglycolysis following TBI with specific emphasis on the changes in neurochemistry, cerebral blood flow and lactate production. The experimental design of this project will address the degree and extent of cerebral blood flow-metabolic uncoupling following TBI and how this relates to cell survival.

Our general hypothesis is that hyperglycolysis, defined in terms of the metabolic ratio between glucose and oxidative metabolism, is a immutable consequence of TBI. Hyperglycolysis is a result of cellular energy demands in direct response to ionic fluxes. This increase in fuel demand results in a metabolic crisis during which cerebral blood flow may not be sufficient and reflects an inefficient production of energy, resulting in the accumulation of lactate. This metabolic crisis defines the degree and extent of injury and provides important insight into explaining why the brain is so vulnerable following TBI.

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