Involvement of excitatory neurotransmitters in the damage produced in chick embryo retinas by anoxia and extracellular high potassium

Chick embryo retinas were exposed for 40 min to anoxic conditions and the resulting histological changes were studied by light microscopy. A strong edematous response with severe swelling of the inner nuclear, inner plexiform and ganglion cell layers and numerous cells with pyknotic nuclei but very few dead cells were observed. These changes were qualitatively similar to those observed on retinas exposed to high potassium concentration [or to glutamic acid. The deleterious effects of anoxia and high potassium concentration] were not affected by the removal of calcium ions from the retina incubation medium but were prevented by γ-d-glutamylglycine, an antagonist of excitatory amino acid receptors. These results suggest that the damage observed in retinas maintained under anoxia for 40 min is likely to be due to the release, from non-synaptic pools, of excitatory neurotransmitters, possibly glutamic and/or aspartic acids, evoked by the dissipation of the membrane ionic gradients. These events would be the first in a chain of toxic damage leading ultimately to cell death.