Observations on the nucleolar and total cell body nucleic acid of injured nerve cells

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Abstract
The nucleic acid content of neuronal nucleoli and the total cell body nucleic acid content of neurons of the hypo-glossal nucleus were measured by UV absorption microspectrography. After nerve injury both the nucleolar nucleic acid and the total cell body nucleic acid increased: nucleolar changes preceded those of the cell body. The closer to the nerve cell body that the axon was injured the earlier was the onset and the decline of the nucleolar response. Actinomycin D was given to prevent DNA-primed RNA synthesis, and the rate of "decay" of nucleolar RNA was measured. This rate varied after nerve injury and was closely related to the nucleolar nucleic acid content. The apparent rate of transfer of labelled RNA from the neuronal nucleus into the cytoplasm changed after nerve injury in a manner closely related to the changes in nucleolar nucleic acid content. It was demonstrated by making consecutive nerve injuries or by preventing or delaying nerve regeneration, that the nucleic acid changes were not induced by removal of contact between the neurone and its motor end-plate, and were not repressed by the restoration of such contact. When regeneration was prevented the nucleolar nucleic acid content and the total cell body nucleic acid ultimately decreased to values less than normal: this decrease was greater when more of the axon was initially removed. The results are discussed in relation to the factor responsible for derepression and repression of DNA cistrons for ribosome synthesis in injured nerve cells.