The effect of local cooling on the sensitivity to noradrenaline of vessels in the feet.
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Biomedical subjects
Publications and source records attributed to G M Bray.
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Axons which lack Schwann cells characterize the spinal roots of dystrophic mice. In these nerves, two types of cells are associated with large axons-typical Schwann cells which ensheath and myelinate individual axons and "uncommitted" cells which closely contact some axons but do not unsheath them normally. Although neonatal Schwann cell multiplication in dystrophic spinal roots is less than normal, the "uncommitted" cells continue to multiply in adult animals. Thus, these cells are presumably responsive to the mitogenic stimulus of axons, but are unable to extend radially and longitudinally to form a myelin sheath. This disorder of axon-sheath cell interactions could be due to an intrinsic abnormality of Schwann cells or a failure of the mechanisms whereby axons induce Schwann cell differentiation.
Peripheral nerves of the mutant mouse Trembler are characterized by a severe myelin deficit and an increased number of Schwann cells. On the basis of radioautographic and quantitative morphologic investigations, the present study documents: i an abnormal persistence of post-natal Schwann cell proliferation in Trembler mouse nerves which, in unaffected animals, are composed of myelinated fibres; ii normal morphology, numbers and proliferation of Schwann cells in the unmyelinated (Remak) fibres of Trembler mice; and iii replication of the increased rate of Schwann cell multiplication as well as the myelin deficit, when segments of Trembler sciatic nerves are transplanted into the sciatic nerves of normal mice. Thus, the continued proliferation of Trembler Schwann cells must be related to the primary inability of these cells to produce and maintain a normal myelin sheath; axonal or general systemic abnormalities do not appear to play a major role in the pathogenesis of these disorders in the Trembler mouse.
Large axons identified in freeze-fracture replicas of the spinal cord white matter of 'shaking pups' were encircled by spiral processes at the paranodes that appeared to arise from oligodendrocytes. In the axolemma adjacent to some of these processes there were paranode-like intramembranous specializations and node-like accumulations of E-face particles; in other instances, no special contacts formed between axons and the spiral processes. The outer surfaces of the spiral processes, which often apposed astrocytes, frequently contained gap junctions. Although many of the abnormalities identified in this dysmyelinating mutant by freeze-fracture electron microscopy are probably secondary to a more fundamental defect of myelin formation, the prominence of the spiral processes suggests that the encircling of axons by oligodendrocytes may be an independent state of ensheathment and not a passive effect of myelin formation.