Degeneration of mouse digital corpuscles

Abstract

The sequential changes of the morphology and the histochemically demonstrated, nonspecific cholinesterase (ChE) activity of the denervated digital corpuscle (Meissner corpuscle) of the mouse were observed by light and electron microscopy for 6 months after transection of the sciatic nerve. A fragment of the sciatic nerve, approximately 1 cm long, was removed from the distal stump to prevent reinnervation. Within one day following nerve division, the axon terminals began to manifest degenerative changes; the axoplasm became electronopaque and some mitochondria became disorganized. The lamellar cell processes (lamellae) also exhibited atrophic changes; they became thinner and more electron opaque. The lamellar cell body became smaller due to a decreased amount of cytoplasm and contained few organelles except for some free ribosomes. These changes advanced with time. Around 4–6 months after denervation, the corpuscle was small, consisting of a few thin, shrunken, atrophic lamellar cells. The ChE activity persisted and could be demonstrated in the interlamellar spaces, but its intensity decreased with time so that the corpuscle was hardly identifiable by light microscope histochemistry around 4–6 months after denervation. During this time, the precipitates of the reaction product were scattered as small particles throughout the interlamellar spaces. The enzyme activity in the cisternae of the rough endoplasmic reticulum and the nuclear envelope of the lamellar cell body was no longer demonstrable 5 days or less after denervation. These findings indicate that the lamellar cell is dependent on the axon terminal to maintain its normal morphology and the function of ChE synthesis.