GLYCINE RECEPTORS IN THE RETINAS OF NORMAL AND SPASTIC MUTANT MICE

Purpose. Spastic mutant mice have abnormal gait and righting behavior, and the responses of their retinal ganglion cells have recently been shown to be abnormal. The former defects have been linked to a reducti on of glycine-receptor density in the spinal cord of spastic mutants, but the cause of the retinal defects has not yet been determined. The authors thus tested for reduced glycine-receptor density in the mutant retina by comparing the levels of glycine receptors in the retinas of spastic mutant mice with those found in normal mice. Methods. Indirec t immunofluorescence histochemistry was employed, using monoclonal ant ibodies directed against the alpha- and beta-subunits of the receptor and against the 93-kd cytoplasmic receptor-associated protein, gephyri n. Results. In normal mice, all glycine-receptor antibodies labeled tw o laminae of the inner plexiform layer (IPL): a broad band in the dist al third of the IPL and a narrow band in the middle of the IPL. Lighte r labeling was also seen in the outer plexiform layer with these antib odies. In spastic mutant mice, the glycine-receptor labeling of the IP L was reduced markedly. However, the overall structure of the spastic mutant retina was not disrupted because the distribution and intensity of both a presynaptic marker (synaptophysin) and a marker for the rod bipolar cell (protein kinase C) in the mutant retina were indistingui shable from those in normal retinas. Conclusions. The glycine-receptor distribution in normal mice was consistent with that previously repor ted for the rat and with the distribution of glycine responsiveness of dissociated rodent bipolar cells. The reduced levels of glycine recep tors in spastic mice help explain the abnormal ganglion cell responses in the spastic mutant.