Extracellular (EC) ascorbate concentrations were measured in microdialysates from the cerebral cortex in rats subjected to cortical compression-contusion trauma. The trauma induced a transient, dramatic increase in EC ascorbate compared to the basal level before the insult and compared to control animals. The data support the presence of a releasable intracellular pool of ascorbate in the neocortex. The possibility that ascorbate may influence traumatic brain damage by its proposed neuromodulatory property and/or by its ability to induce lipid peroxidation is considered.