Degeneration and phagocytosis of synaptic endings and axons in the medial trapezoid nucleus of the cat

Abstract

AbstractThis study deals with the fine structure of the degenerative changes in the axonal calyces of the medial trapezoid nucleus after destruction of their cell bodies of origin in the contralateral cochlear nucleus. Two to four days after such lesions the main calycine processes which normally contain a core of neurofilaments, show a marked hyperplasia of neurofilaments, shrinkage, decrease in number of microtubules and mitochondria, swelling and decrease in number of synaptic vesicles, and the appearance of vesicular debris and coated vesicles. After seven days all of the calyces have degenerated. They are replaced by extracellular accumulations of neurofilaments, surrounded by phagocytic processes of proliferating astroglia and microglia. In contrast, the calycine appendages exhibit a dense mode of degeneration. Thus the different kinds of endings, arising from the very same fibers and synapsing on the very same cell bodies, exhibit two entirely different modes of degeneration. There is a correlation between the normal cytological features of the endings and their modes of degeneration. The preterminal calycine axons undergo filamentous hyperplasia in early degeneration.The observations indicate that both microglia and astroglia may participate in phagocytosis of the preterminal fibers and their endings and that astrocytes undergo mitosis. The microglia in electron micrographs correspond to the classical microglial cells that appear in perivascular locations in Golgi preparations. The disintegration of the calyces is accompanied by mutual invaginations of thin axonal and glial processes, followed by the disappearance of the axolemma. Extracellular break‐up appears to be a regular feature of this process, which may involve the intercellular transfer of soluble breakdown products by calycine and glial vesicles and uptake by tubular elements of the smooth endoplasmic reticulum in the phagocytes. Incisures of Schmidt‐Lanterman occur in the large calyciferous fibers; these fibers are often invaded by phagocytes before the myelin sheath degenerates.