Alterations in the compartmentalized metabolism of glutamic acid with changed cerebral conditions.

Data obtained from combined determinations of the nervous tissue content of glutamic acid, taurine and glutamine were examined in terms of the well established concept of a compartmentalized metabolism for glutamic acid. Three different situations associated with altered cortical conditions were studied: cortical hyperexcitability induced by cobalt epilepsy (mouse); chronic stimulation of the optic tectum by light adaptation (fish); and anatomic alteration of the optic tectum following unilateral enucleation (fish). All 3 situations appear to cause a reduction in the ability of glial elements to capture free glutamic acid released from neuronal structures. However, the underlying causes for such an insufficiency seem to differ in each instance. In epilepsy the release of glutamic acid and taurine exceeds the glial capture rate; during chronic stimulation of a normal cortex a diminished glial uptake rate for both amino acids seems apparent; anatomical degenerative changes seem to diminish especially the glutamine retention capacity of the cortex, possibly in combination with a reduced glial taurine uptake.