A light and electron microscopic study of the cellular response to axonal injury in the superior cervical ganglion of the rat
- 18 April 1972
- journal article
- Published by The Royal Society in Proceedings of the Royal Society of London. B. Biological Sciences
- Vol. 181 (1062) , 43-79
- https://doi.org/10.1098/rspb.1972.0040
Abstract
Postganglionic branches were ligated or cut 1 to 2 mm from the ganglion in 48 Wistar rats. The ganglia were examined at intervals from 6 h to 143 days. Light microscopy showed chromatolysis of Nissl material involving up to 85% of ganglionic neurons by 24 h. Up to 60% of neurons were still chromatolytic after 21 days. Chromatolysis in the reacting neurons was accompanied by central aggregation of dense bodies, displacement and indentation of the nucleus and increased staining of the nuclear rim. Electron microscopy showed significant increases, in the cell bodies of reacting neurons 3 to 14 days postoperatively, in numbers of autophagic vacuoles and of a sequence of forms of cytoplasmic dense bodies (which became more complex in form, and developed stacks of linear densities and whorls). Later the dense bodies reverted to a more normal appearance but showed frequent lipofuscin droplets. There were signs of phagocytosis of neuronal cytoplasm by sheath cells. Significant decreases were found in the incidence in cell bodies of reacting neurons, 3 to 14 days postoperatively, of large (80 to 110 nm) dense-cored vesicles, of clumps of small vesicles (some with dense cores) and of the regular form of multivesicular body. All these organelles accumulate in the proximal stumps of the ligated axons. There was also an increasing tendency in reacting neurons to marginal aggregation of the nuclear chromatin. From 2 days postoperatively there was evidence of sprouting from axons and cell bodies. It was concluded that the neuron in chromatolysis undergoes a form of partial involution, which may relate more to its transmitter and receptive functions than to processes concerned with regrowth of the axon.Keywords
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