Abstract
Neuronal activity is accompanied by transmembranous ion fluxes that cause cell volume changes. In whole mounts of the guinea pig retina, application of glutamate resulted in fast swelling of neuronal cell bodies in the ganglion cell layer ( GCL) and the inner nuclear layer ( INL) ( by -40%) and a concomitant decrease of the thickness of glial cell processes in the inner plexiform layer ( IPL) ( by -40%) that was accompanied by an elongation of the glial cells, by a thickening of the whole retinal tissue, and by a shrinkage of the extracellular space ( by -18%).
The half-maximal effect of glutamate was observed at -250 muM, after -4 min. The swelling was caused predominantly by AMPA kainate receptor-mediated influx of Na+ into retinal neurons.
Similar but transient morphological alterations were induced by high K+ and dopamine, which caused release of endogenous glutamate and subsequent activation of AMPA-kainate receptors. Apparently, retinal glutamatergic transmission is accompanied by neuronal cell swelling that causes compensatory morphological alterations of glial cells.
The effect of dopamine was elicitable only during light adaptation but not in the dark, and glutamate and high K+ induced stronger effects in the dark than in the light. This suggests that not only the endogenous release of dopamine but also the responsiveness of glutamatergic neurons to dopamine is regulated by light-dark adaptation.
Similar morphological alterations ( neuronal swelling and decreased glial process thickness) were observed in whole mounts isolated immediately after experimental retinal ischemia, suggesting an involvement of AMPA-kainate receptor activation in putative neurotoxic cell swelling in the postischemic retina.