The diameter of cell nuclei and mean volume of internuclear material p e r nucleus were determined in the auditory cortex in growing and adult mice. The influence of stay in complete darkness for 2-4 months was investigated.In growing mice, a decrease in nuclear size and relative volume of internuclear material was observed after two months in the dark from birth. Prolonged stay in the dark caused an increase in nuclear size and internuclear material, and the hypotrophy of the auditory cortex was succeeded by hypertrophy after four months in the dark from birth. In adult mice, reared in darkness for three months from four to seven months of age, similar hypertrophy of the auditory cortex was recorded.Compared to the findings in the striate cortex of visually deprived mice (in a previous investigation), the initial hypotrophy of the auditory cortex after visual deprivation was less pronounccd than the hypotrophy observed in the visual cortex. In the latter, n o late hypertrophy occurred after prolonged stay in the dark, and hypotrophy was found in the adult, visually deprived mice, and not hypertrophy as in the auditory cortex. The possibility of compensatory auditory training and cortical hypertrophy is discussed.

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The thickness of the visual cortex, the diameter of cell nuclei and the mean volume of internuclear material per nucleus in the visual cortex, geniculate bodies and superior colliculi were determined in growing and adult mice. The influence of prolonged stay in complete darkness was investigated.In the visual cortex of normal mice, a peak in nuclear size occurred 20-30 days after birth, followed by a peak in relative volume of internuclear material.In growing mice, reared in darkness from birth, a highly significant decrease in relative volume of internuclear material occurred in all visual centers. The decrease was greatest in the geniculate bodies and greater in the granular and supragranular layers of the cortex than in the infragranular. In the cortex, the decrease was most pronounced after two months and became less pronounced during prolonged stay in darkness. No similar normalization was observed in subcortical visual centers. In the same mice, visual deprivation caused a highly significant decrease in the thickness of the visual cortex and in the diameter of its cell nuclei. The dgcrease in nuclear diameter was greater in the granular and supragranular than in the infragranular layers of the cortex and exhibited a similar normalization during prolonged stay in darkness as the decrease in relative volume of internuclear material.In adult mice, visual deprivation caused decrease in internuclear material.

Summary1. Newborn, full‐term mice were subjected to exposures in 98–100 per cent oxygen,(a) intermittently, (b)continuously, or (c)for five days followed by rapid transfer to, and stay in, normal atmosphere. The development of the eyes was followed histologically for 38, 16, and 15 days after birth, respectively.2. Intermittent exposures to oxygen caused a high frequency of persistence, proliferation and dilatation of the retrolental hyaloid vessels with hemorrhages in the primary vitreous body. Eetinal folds were occasionally found.3. Continuous exposures to oxygen caused a persistence and proliferation of the retrolental hyaloid vessels and a retarded formation of retinal vessels. Small intraocular blecdings occurred occasionally.4. Continuous exposures to oxygen followed by rapid transfer to, and stay in, normal atniosphere caused a dilatation and a progressive proliferation of the retrolental hyaloid vessels and of retinal vessels with capillary buddings from the retinal vessels into the vitreous body. Hemorrhages from both retinal and hyaloid vessels occurred frequently. The retina showed progressive irregularities, proliferations and foldings.5. netinal atrophy after longer periods of observation since the transfer from oxygen to normal air is preliminarily reported.6. The experimental changes of the eyes after oxygen exposures are discussed with regard to the patliogenesis of human retrolental fibroplasia.