Toru Tamura

TL;DR: The data suggest that concussive brain injury causes a massive K+ flux which is likely to be related to an indiscriminate release of excitatory amino acids occurring immediately after brain injury.

TL;DR: Findings suggest that Ca(2+)-dependent exocytotic release from the presynaptic nerve terminals is involved predominantly in the earlier rapid increase in [Glu]d, which may be due in part to a breakdown of membrane function resulting from several causes, including a loss of the electrogenic component of the glutamate gradients across the plasma membrane.

TL;DR: The findings indicate that the early cellular swelling occurring during cerebral ischemia is a result of massive ionic fluxes mediated by excitatory amino acids which are released by a Ca(2+)-dependent exocytotic process from the nerve terminals.

TL;DR: Early cellular swelling following fluid-percussion brain injury was demonstrated in vivo by means of microdialysis in the rat as a result of ionic fluxes mediated by EAAs.

TL;DR: The physiological features and limitations of K(+)-free dialysis used to detect changes in extracellular concentration of K+ in the rat hippocampus in vivo are characterized and the hypothesis that the initial increase in [K+]e during cerebral ischemia is related to the Ca(2+)-dependent exocytotic release of neurotransmitters from depolarized nerve terminals is consistent.