Retardation of schwann cell division and axonal regrowth following nerve crush in experimental lead neuropathy

In experimental lead neuropathy, Schwann cells undergo segmental demyelination and possibly cell death and, concurrently, remyelination and multiplication to create new internodes of myelin and onion bulb formations. In rats fed 4% lead carbonate for three months, the ability of Schwann cells to divide (percentage showing mitotic figures, labeling index, and total number per millimeter of fascicular length of nerve) was studied serially for four weeks. Schwann cell events were also compared in sural nerve distal to crush with and without resection of an intervening length of nerve. In both cases, Schwann cell multiplication as a result of axotomy was retarded in lead‐intoxicated as compared to control animals. On the average, regrown myelinated axons four weeks after and 10 mm below the point of crush in lead‐treated animals were similar in number and smaller in caliber, but they exhibited a normal relationship of myelin thickness to axonal area compared with control animals. These studies provide evidence that Schwann cell division and axonal regrowth after crush are retarded in experimental lead neuropathy.

[1]  P. Dyck,et al.  Human diabetic endoneurial sorbitol, fructose, and myo‐inositol related to sural nerve morphometry , 1980, Annals of neurology.

[2]  P. Dyck,et al.  Structural and Biochemical Effects of Essential Fatty Acid Deficiency on Peripheral Nerve , 1980, Journal of neuropathology and experimental neurology.

[3]  A. Windebank,et al.  The Endoneurial Content of Lead Related to the Onset and Severity of Segmental Demyelination , 1980, Journal of neuropathology and experimental neurology.

[4]  A. Windebank,et al.  Blood Nerve Barrier in Rat and Cellular Mechanisms of Lead‐induced Segmental Demyelination , 1980, Journal of neuropathology and experimental neurology.

[5]  Gibson Jd.  The origin of the neural macrophage: a quantitative ultrastructural study of cell population changes during Wallerian degeneration. , 1979 .

[6]  D. Price,et al.  Chronic lead intoxication: Effects on developing optic nerve , 1979, Annals of neurology.

[7]  P. Spencer,et al.  An in vivo method to prepare normal Schwann cells free of axons and myelin , 1979, Brain Research.

[8]  W. Blumberg.  Enzymic modification of environmental intoxicants: the role of cytochrome P–450 , 1978, Quarterly Reviews of Biophysics.

[9]  B. Fowler.  General subcellular effects of lead, mercury, cadmium, and arsenic. , 1978, Environmental health perspectives.

[10]  P. Dyck,et al.  Increased endoneurial fluid pressure in experimental lead neuropathy , 1977, Nature.

[11]  P. Dyck,et al.  LEAD NEUROPATHY: 1) MORPHOMETRY, NERVE CONDUCTION, AND CHOLINE ACETYLTRANSFERASE TRANSPORT NEW FINDING OF ENDONEURIAL EDEMA ASSOCIATED WITH SEGMENTAL DEMYELINATION , 1977, Journal of neuropathology and experimental neurology.

[12]  P. Dyck,et al.  LEAD NEUROPATHY: 2. RANDOM DISTRIBUTION OF SEGMENTAL DEMYELINATION AMONG “OLD INTERNODES” OF MYELINATED FIBERS , 1977, Journal of neuropathology and experimental neurology.

[13]  P. Dyck,et al.  Studies to improve fixation of human nerves Part 3. Effect of osmolality of glutaraldehyde solutions on relationship of axonal area to number of myelin lamellae , 1976, Journal of the Neurological Sciences.

[14]  A. Aguayo,et al.  Schwann cell multiplication after crush injury of unmyelinated fibers. , 1976, Archives of neurology.

[15]  A. Aguayo,et al.  Experimental necrosis and arrest of proliferation of Schwann cells by cytosine arabinoside , 1975, Journal of neurocytology.

[16]  R. Bunge,et al.  Evidence that sensory axons are mitogenic for Schwann cells , 1975, Nature.

[17]  C. A. Stirling.  Experimentally induced myelination of amyelinated axons in dystrophic mice , 1975, Brain Research.

[18]  N. Gregson,et al.  THE EFFECTS OF MITOMYCIN C ON THE PROCESS OF REMYELINATION IN THE MAMMALIAN PERIPHERAL NERVOUS SYSTEM , 1975 .

[19]  R. Goyer,et al.  Lead-Induced Inclusion Bodies: Composition and Probable Role in Lead Metabolism , 1974, Environmental health perspectives.

[20]  E. Hogan,et al.  LEAD ENCEPHALOPATHY IN THE DEVELOPING RAT: EFFECT UPON MYELINATION , 1974, Journal of neuropathology and experimental neurology.

[21]  J. Morgan-Hughes,et al.  The pattern of peripheral nerve regeneration induced by crush in rats with severe acrylamide neuropathy. , 1974, Brain : a journal of neurology.

[22]  N. Gregson,et al.  A quantitative analysis of the effects of the intraneural injection of lysophosphatidyl choline. , 1973, Journal of cell science.

[23]  W. Bradley,et al.  RADIOAUTOGRAPHIC STUDIES OF SCHWANN CELL BEHAVIOR: I. ACRYLAMIDE NEUROPATHY IN THE MOUSE , 1970, Journal of neuropathology and experimental neurology.

[24]  R. Goyer,et al.  Lead dosage and the role of the intranuclear inclusion body. An experimental study. , 1970, Archives of environmental health.

[25]  Thomas Pk.  The cellular response to nerve injury. 3. The effect of repeated crush injuries. , 1970 .

[26]  W. Bradley,et al.  Duration of synthesis phase in neuilemma cells in mouse sciatic nerve during degeneration. , 1970, Experimental neurology.

[27]  S. Levine,et al.  INTRAMYELINIC AND EXTRACELLULAR SPACES IN TRIETHYLTIN INTOXICATION , 1968, Journal of neuropathology and experimental neurology.

[28]  B. Arnason,et al.  Experimental allergic neuritis: a radioautographic study. , 1968, Journal of neuropathology and experimental neurology.

[29]  P. Lampert,et al.  Demyelination and remyelination in lead neuropathy. Electron microscopic studies. , 1968, Journal of neuropathology and experimental neurology.

[30]  J. Cavanagh.  Effects of x-irradiation on the proliferation of cells in peripheral nerve during Wallerian degeneration in the rat. , 1968, The British journal of radiology.

[31]  A. Asbury.  SCHWANN CELL PROLIFERATION IN DEVELOPING MOUSE SCIATIC NERVE , 1967, The Journal of cell biology.

[32]  Thomas Pk.  The cellular response to nerve injury. 1. The cellular outgrowth from the distal stump of transected nerve. , 1966 .

[33]  H. Waldron.  The Anaemia of Lead Poisoning: A Review , 1966, British journal of industrial medicine.

[34]  D. Pease,et al.  REGENERATIVE CHANGES IN RAT DORSAL ROOTS FOLLOWING WALERIAN DEGENERATION. , 1963, Journal of ultrastructure research.

[35]  S. Gelfant.  INHIBITION OF CELL DIVISION: A CRITICAL AND EXPERIMENTAL ANALYSIS. , 1963, International review of cytology.

[36]  M. Abercrombie,et al.  An analysis of growth in nuclear population during Wallerian degeneration. , 1957, Journal of cellular and comparative physiology.

[37]  J. Joseph.  FURTHER STUDIES IN CHANGES OF NUCLEAR POPULATION IN DEGNERATING NON-MYELINATED AND FINELY MYELINATED NERVES , 1950 .

[38]  Thomas Ga.  Quantitative histology of Wallerian degeneration: II. Nuclear population in two nerves of different fibre spectrum. , 1948 .

[39]  M. Abercrombie,et al.  Quantitative histology of Wallerian degeneration: I. Nuclear population in rabbit sciatic nerve. , 1946, Journal of anatomy.