Injections of leupeptin (a thiol proteinase inhibitor) or chloroquine (a general lysosomal enzyme inhibitor) into the brains of young rats induced the formation of lysosome-associated granular aggregates (dense bodies) which closely resembled the ceroid-lipofuscin that accumulates in certain disease states and during aging. The dense material increased in a dose- and time-dependent fashion and was differentially distributed across brain regions and cell types. These observations provide clues to the origins of ceroid-lipofuscin and suggest means for studying the consequences of its accumulation.

Development changes in the origins of contra- and ipsilateral projections from the rat parietal cortex were examined using the retrograde transport of horseradish peroxidase and of the fluorescent dyes fast blue and nuclear yellow. The aim of the study was to determine the fate of the neurons which send axons through the corpus callosum in the neonatal, but not the young adult, rat. 1. Neurons which project across the corpus callosum at postnatal day 8 (PND 8), but not at PND 20 or later, do not die; they merely lose their contralateral processes. 2. At PND 8, many of these neurons--in particular, those in lamina Va of the barrel field area--project simultaneously across the corpus callosum and to the ipsilateral motor cortex. 3. By PND 20 and later, many neurons in lamina Va of the barrel field area still project to the ipsilateral motor cortex but not across the corpus callosum. We conclude that at least some neocortical neurons initially elaborate more axonal processes than they will maintain and that they selectively eliminate major projections during development.