An electron microscopic study of the modification by monosodium glutamate of the retinas of normal and “rodless” mice

Sodium‐L‐glutamate was administered to post‐natal Swiss albino and agouti C3H/HeJ “rodless” mice. In both cases there was at two months a marked reduction in myelinated axons of the optic nerve from about 25,000 to less than 225 axons but Swiss mice had more ganglion cell somas than axons. Glutamate‐treated eyes seemed smaller and the lenses were 65% of the weight of control lenses. The inner nuclear layer of Swiss‐glutamate retinas was reduced from 5–7 nuclei deep to 1–2. In treated Swiss mice the receptor concentration appears unchanged and electron microscopy revealed that both spheroidal and pedicular receptor terminals were contacted by presumed neurites of second order neurons. There was a small, relative increase in terminals of bipolar neurons in the markedly reduced inner plexiform layer. Relative to these findings a description is given of normal synaptic arrangements. In glutamate‐treated “rodless” mice at two months the retina contained two rows of nuclei. Imbricated processes of glial cells of Müller faced the pigment epithelium and the retina contained scattered ganglion cells, bipolar cells, and other neurons less readily characterized. At two months most glutamate‐treated mice, rod containing or “rodless,” had a direct pupillary response and a detectable but obviously weaker consensual response. Preliminary examinations of animals one year after glutamate treatment showed receptor deterioration in albino animals and further retinal deterioration in both groups. The two surviving C3H‐glutamate animals possessed milky cataractous lenses, however full but sluggish direct iris constrictions could be elicited.