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Electron microscopic studies of the dentate gyrus of the rat. II. Degeneration of commissural afferents
Author(s) -
Laatsch R. H.,
Cowan W. M.
Publication year - 1967
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.901300306
Subject(s) - axon , biology , dentate gyrus , neurofilament , axoplasmic transport , axoplasm , granule cell , dendritic spine , electron microscope , anatomy , free nerve ending , neuroscience , central nervous system , hippocampal formation , immunohistochemistry , immunology , physics , optics
Experimental degeneration of the commissural afferents to the dentate gyrus of the rat has been studied using the electron microscope. Four and six days after unilater fimbrial section, unequivocal degeneration of axon terminals is found in the inner part of the molecular layer of the dentate gyrus of the opposite side. The affected endings are in synaptic contact both with the shafts of the granule cell dendrites and with the short dendritic spines which occur on the granule cell dendrites in this part of the molecular layer. These degenerating terminals show changes ranging from an increased axoplasmic density with aggregation of the synaptic vesicles, to a complete disappearance of the vesicles and mitochondria, and the engulfment of the endings by glycogen‐containing processes of glial cells. There is no proliferation of neurofilaments at any stage during this degeneration. Glial processes in the vicinity of degenerating axon terminals show reactive changes in the form of swelling and accumulation of glycogen, and probably proceed to phagocytosis of the degenerating nerve endings. On the side of the lesion the glial cells also show fibril proliferation, an even greater accumulation of glycogen, and a variety of ingested cellular debris.