The axotomy response

Abstract

The classic though not invariable signature of the axotomy response (axon reaction) in peripheral (extrinsic) neurons is that of central chromatolysis, a cytologic phenomenon exhibited by the cell body and studied repeatedly by neurobiologists for more than a century. Central chromatolysis occurs almost exclusively in response to axon injury and is present in many but not all axotomized peripheral neurons, though transiently and acutely [ [1] Barron K.D Axon reaction and central nervous system regeneration. in: Seil F.J Nerve, organ and tissue regeneration: research perspectives. Academic Press, New York1983: 3-36 Crossref Google Scholar ], unless axonic regeneration is impeded, as by nerve ligature. It is marked by rounding and (often) enlargement of the soma and nucleus, disaggregation and peripheral dispersion of the somal ribonucleoprotein aggregates (which came to bear Nissl's name) and clearing of the cytocentrum. Breakup and retispersion of the Golgi apparatus occur also. Nissl described the changes in the aggregation and distribution of Nissl substance in 1892 (cited in [2] Lieberman A.R The axon reaction: a review of the principal features of perikaryal responses to axon injury. Int. Rev. Neurobiol. 1971; 14: 49-124 Crossref PubMed Scopus (948) Google Scholar ) after thiazine dyes became available to histologists. In a masterly and widely cited review, Lieberman [ [2] Lieberman A.R The axon reaction: a review of the principal features of perikaryal responses to axon injury. Int. Rev. Neurobiol. 1971; 14: 49-124 Crossref PubMed Scopus (948) Google Scholar ] commented on the “very few studies” that had been directed to the elucidation of the axotomy response in central (intrinsic) nerve cells. Although central chromatolysis occurs in a minority of central neurons after axotomy, the axon reaction in these cells goes on generally and promptly to cellular atrophy and loss of basophilia [ [3] Barron K.D Neuronal responses to axotomy: consequences and possibilities for rescue from permanent atrophy or cell death. in: Seil F.J Neural regeneration and transplantation. Liss, New York1989: 79-99 Google Scholar ]. In contrast, the axotomy response in peripheral neurons is followed generally by recovery to the preaxotomy state. However, in both classes of neurons, cell death may result. Important variables affecting the axotomy response include age and species of the subject, manner of production of axotomy (e.g., transection vs. crushing injury), distance of the injury site from the parent soma and, related to this last, sparing of collaterals proximal to the axonic interruption. Concomitant deafferentation [ [1] Barron K.D Axon reaction and central nervous system regeneration. in: Seil F.J Nerve, organ and tissue regeneration: research perspectives. Academic Press, New York1983: 3-36 Crossref Google Scholar ] as by brain lesions causing both deafferentation and axotomy (e.g., the thalamus after corticectomy) increases the severity of the axotomy response.