PubMed Health⌕ Search

Biomedical subjects

G M Bray

Publications and source records attributed to G M Bray.

At least 73 records · Page 4Linked to original sources
PubMed1975

Experimental necrosis and arrest of proliferation of Schwann cells by cytosine arabinoside.

In developing rat cervical sympathetic trunks, Schwann cells proliferate intensely during the first week after birth but axonal populations do not increase. Thus, experimental inhibition of DNA synthesis should affect Schwann cells and spare axons whose cell bodies are not dividing. The present investigation was aimed at determining the effects of an inhibitor of DNA synthesis-cytosine arabinoside (ara-C)--on axons and Schwann cells in developing nerves. Ara-C (60 mg kg(-1) body weight) was injected subcutaneously to newborn rats every six hours for 36 hours. At intervals from 2--4 days of age, animals were given tritiated thymidine (4 muCi per gram body weight) to label Schwann cells in synthesis phase. One hour later rats were killed by systemic perfusion of phosphate buffered glutaraldehyde. Cervical sympathetic trunks (CST's) and sciatic nerves were removed and processed for radioautography and electron microscopy (EM). Labelled and unlabelled Schwann cell nuclei were counted to determine the labelling index (LI%) for each nerve. By the end of ara-C treatment there was almost complete absence of labelling but LI's rose sharply 24 hours after discontinuing ara-C. By EM axons appeared normal; Schwann cells, however, showed prominent nuclear and cytoplasmic changes consisting of nuclear degeneration, dilatation of rough endoplasmic reticulum and increased cytoplasmic density. Ara-C, by suppressing proliferation and causing necrosis of Schwann cells but sparing axons, results in a developmental alteration of axon-Schwann cell relationships. It is suggested that the pathogenetic mechanism involves an inbalance in DNA/RNA synthesis metabolism.

Animals↗
PubMed1975

Quantitative ultrastructural studies of the axon Schwann cell abnormality in spinal nerve roots from dystrophic mice.

Lumbo-sacral spinal roots and the nerve to the medial gastrocnemius muscle (NMG) from normal and dystrophic mice were examined by quantitative ultrastructural techniques. It was demonstrated that, although many axons at this level were totally devoid of Schwann cells, totatl axonal numbers were approximately normal. Some axons in these roots were surrounded by Schwann cells but their myelin sheaths were abnormally thin. In addition, cells resembling oligodendrocytes were observed in the dorsal roots of the dystrophic mice. In contrast, Schwann cells and myelin sheaths were normal in the more peripherally situated NMG and the regenerative response of these nerves to crush injury was not significantly different from that of control nerves. Thus, the main abnormality of neural morphology in dystrophic mice is a localized absence of Schwann cells. Such a deficiency does not appear to have influenced axonal growth or the capacity of these axons to regenerate when crushed distally.

Animals↗