Release of excitatory amino acids in the penumbra of a focal cortical necrosis.

A cortical tissue necrosis from focal trauma expands between 30% and 300% from its initial size within 24 h, depending on the species studied. To shed light on the pathophysiological processes in the penumbra 1 zone after a focal cortical lesion, the release of excitatory amino acids into the traumatic penumbra zone 1 was measured throughout the entire period of necrosis expansion. A microdialysis probe was inserted at an oblique angle into the cortex of Sprague-Dawley rats 2 mm below the brain surface. One day later, a highly standardized cortical freezing lesion was induced at the brain cortex above the microdialysis probe. Dialysate was continuously collected prior to, during, and up to 24 h after trauma and analyzed for primary amino acids. In each animal, it was confirmed histologically that the tip of the microdialysis probe was localized in the gray matter in close proximity to the primary lesion. Following induction of the trauma, a statistically significant sharp increase of the dialysate level of aspartate, glutamate, glycine, and serine was observed. Thereafter, the dialysate levels of these amino acids returned to baseline levels without any further increase throughout the remaining observation period. This process ranged in time from a few minutes to a few hours. The level of alanine in the dialysate was essentially not altered throughout the experiment. Although the early post-traumatic increase of the excitatory neurotransmitters aspartate and glutamate may well contribute to the secondary lesion growth of a cortical necrosis after trauma, glutamate receptor targeted therapeutic intervention may be in view of these findings of limited use when initiated post trauma.