Increased expression of neuronal glucose transporter 3 but not glial glucose transporter 1 following severe diffuse traumatic brain injury in rats

Traumatic brain injury results in an increased brain energy demand that is associated with profound changes in brain glycolysis and energy metabolism. Increased glycolysis must be met by increasing glucose supply that, in bra in, is primarily mediated by two members of the facilitative glucose transp orter family, Glut1 and Glut3. Glut1 is expressed in endothelial cells of t he blood-brain barrier (BBB) and also in glia, while Glut3 is the primary g lucose transporter expressed in neurons. However, few studies have investig ated the changes in glucose transporter expression following traumatic brai n injury, and in particular, the neuronal and glial glucose transporter res ponses to injury. This study has therefore focussed on investigating the ex pression of the glial specific 45-kDa isoform of Glut1 and neuronal specifi c Glut3 following severe diffuse traumatic brain injury in rats. Following impact-acceleration injury, Glut3 expression was found to increase by at le ast 300% as early as 4 h after induction of injury and remained elevated fo r at least 48 h postinjury. The increase in Glut3 expression was clearly ev ident in both the cerebral cortex and cerebellum. In contrast, expression o f the glial specific 45-kDa isoform of Glut1 did not significantly change i n either the cerebral cortex or cerebellum following traumatic injury. We c onclude that increased glucose uptake after traumatic brain injury is prima rily accounted for by increased neuronal Glut 3 glucose transporter express ion and that this increased expression after trauma is part of a neuronal s tress response that may be involved in increasing neuronal glycolysis and a ssociated energy metabolism to fuel repair processes.