Desmielinização tóxica do sistema nervoso central: II. Aspectos biológicos das células de Schwann observados durante o processo de reparação do tecido

Graça, Dominguita Lühers

doi:10.1590/S0004-282X1989000300002

Resumos

A droga gliotóxica brometo de etídio, Quando injetada localmente na medula espinhal do rato, induziu áreas de desmielinização que se desenvolveram em tempos diferentes de acordo com a dose empregada. Doses altas induziram lesões de desenvolvimento rápido (tipo I) e intermediárias (tipo III), enquanto doses baixas induziram lesões lentas (tipo II). Após o processo desmielinizante, os axônios desprovidos de suas bainhas de mielina foram remielinizados por oligodendrócitos ou células de Schwann (CS) dependendo de sua localização em áreas contendo ou não astrócitos, respectivamente. Na maioria das lesões, a área remielinizada pelas CS era proeminente. Nas lesões que repararam mais lentamente foi possível observar os fatores que influenciaram o comportamento dessas células dentro dos limites do sistema nervoso central. Após a invasão inicial a partir da superfície pial e dos espaços perivasculares, a expansão das CS dependeu da presença de matriz extracelular estável. Nas lesões de tipo I, esta matriz estava presente devido à natureza inflamatória do processo. Nas lesões de tipo II a matriz não ocorreu e as CS só podiam migrar entre os axônios desmie-lizados usando-os tal como uma passadeira. Entre as células contíguas podiam ser observadas fibras colágenas de diâmetro pequeno. Não foi evidenciada migração das CS ao longo dos axônios.

The gliotoxic chemical ethidium bromide when injected locally in the rat spinal cord induced areas of demyelination which developed at various times according to the dose used. High doses induced lesions of fast development (type I) and intermediate lesions (type III) whereas low doses induced slow lesions (type II). Following the demyeli-nating process, naked axons were remyelinated either by oligodendrocytes or Schwann cells (SC) depending on their location in areas respectively with or without astrocytes. In most lesions the area remyelinated by SC was proeminent. In lesions of slow development it was possible to observe the factors that influenced SC behavior within the central nervous system. Following the initial invasion from subpial areas and perivascular spaces, SC expansion depended on the presence of a stable extracellular matrix. In type I lesions this matrix was present due to the inflammatory nature of the process. In tipe II lesions that matrix did not occur thus SC only could migrate among demyelinated axons using them as stepping stones. Between adjacent SC thin diameter collagen fibres could be detected. It was not found any evidence of SC migration along the naked axons.

Desmielinização tóxica do sistema nervoso central: II. Aspectos biológicos das células de Schwann observados durante o processo de reparação do tecido

Toxic demyelination of the central nervous system: II. Biological aspects of Schwann cells observed during the process of tissue repair

Dominguita Lühers Graça

Departamento de Patologia, Universidade Federal de Santa Maria: DMV, PhD, Professor Adjunto

RESUMO

A droga gliotóxica brometo de etídio, Quando injetada localmente na medula espinhal do rato, induziu áreas de desmielinização que se desenvolveram em tempos diferentes de acordo com a dose empregada. Doses altas induziram lesões de desenvolvimento rápido (tipo I) e intermediárias (tipo III), enquanto doses baixas induziram lesões lentas (tipo II). Após o processo desmielinizante, os axônios desprovidos de suas bainhas de mielina foram remielinizados por oligodendrócitos ou células de Schwann (CS) dependendo de sua localização em áreas contendo ou não astrócitos, respectivamente. Na maioria das lesões, a área remielinizada pelas CS era proeminente. Nas lesões que repararam mais lentamente foi possível observar os fatores que influenciaram o comportamento dessas células dentro dos limites do sistema nervoso central. Após a invasão inicial a partir da superfície pial e dos espaços perivasculares, a expansão das CS dependeu da presença de matriz extracelular estável. Nas lesões de tipo I, esta matriz estava presente devido à natureza inflamatória do processo. Nas lesões de tipo II a matriz não ocorreu e as CS só podiam migrar entre os axônios desmie-lizados usando-os tal como uma passadeira. Entre as células contíguas podiam ser observadas fibras colágenas de diâmetro pequeno. Não foi evidenciada migração das CS ao longo dos axônios.

SUMMARY

The gliotoxic chemical ethidium bromide when injected locally in the rat spinal cord induced areas of demyelination which developed at various times according to the dose used. High doses induced lesions of fast development (type I) and intermediate lesions (type III) whereas low doses induced slow lesions (type II). Following the demyeli-nating process, naked axons were remyelinated either by oligodendrocytes or Schwann cells (SC) depending on their location in areas respectively with or without astrocytes. In most lesions the area remyelinated by SC was proeminent. In lesions of slow development it was possible to observe the factors that influenced SC behavior within the central nervous system. Following the initial invasion from subpial areas and perivascular spaces, SC expansion depended on the presence of a stable extracellular matrix. In type I lesions this matrix was present due to the inflammatory nature of the process. In tipe II lesions that matrix did not occur thus SC only could migrate among demyelinated axons using them as stepping stones. Between adjacent SC thin diameter collagen fibres could be detected. It was not found any evidence of SC migration along the naked axons.

Texto completo disponível apenas em PDF.

Full text available only in PDF format.

Agradecimentos - A assistência técnica de Irene LLoyd, Robert Patterson (University of Campridge) e Iara Ethur Flores (UFSM) é calorosamente reconhecida.

Departamento de Patologia, Universidade Federal de Santa Maria - Caixa Postal 5092, Balcão Postal UFSM - 91179 Santa Maria RS - Brasil.

1. Beck DW, Hart MN, Cancilla PA - The role of the macrophage in microvascular regeneration following brain injury. J Neuropath Exp Neurol 42: 601, 1983.
2. Blakemore WF - Remyelination by Schwann cells of axons demyelinated by intraspinal injection of 6-aminonicotinamide in the rat. J Neurocyt 4: 745, 1975.
3. Blakemore WF - Invasion of Schwann cells into the spinal cord of the rat following local injections of lysolecithin. Neuropath Appl Neurobiol 2: 21, 1976.
4. Blakemore WF - Ethidium bromide induced demyelination in the spinal cord of the cat. Neuropath Appl Neurobiol 8: 365, 1982.
5. Blakemore WF, Crang AJ - The use of cultured autologous Schwann cells to remyelinate areas of persistent demyelination in the central nervous system. J Neurol Sci 70: 207. 1985.
6. Blakemore WF, Eames RA, Smith KJ, McDonald WI - Remyelimation in the spinal cord of the cat following intraspinal injections of lysolecithin. J Neurol Sci 33: 31, 1977.
7. Blakemore WF, Patterson RC - Suppression of remyelination in the CNS by X-irradiation. Acta Neuropath (Berlin) 42: 105, 1978.
8. Bunge RP, Bunge MB - Evidence that contact with connective tissue matrix is required for normal interaction between Schwann cells and nerve fibres. J Cell Biol 78: 943, 1978.
9. Bunge RP, Bunge MB, Cochran M - Some factors influencing the proliferation and differentiation of myelin-forming cells. Neurology 28:59, 1978.
10. Folkman J - Angiogenesis: initiation and control. Ann NY Acad Sci 401: 212, 1982.
11. Graça DL - Investigation into ethidium bromide induced demyelination in the central nervous system. PhD Thesis, University of Cambridge, UK. Cambridge, 1986.
12. Graça DL, Blakemore WF - Delayed remyelination in rat spinal cord following ethidium bromide injection. Neuropath Appl Neurobiol 12: 593, 1986.
13. Polverini PJ, Cotran RS, Gimbrone MA Jr, Unanue ER - Activated macrophages induce vascular proliferation. Nature 269: 804, 1977.
14. Sanes JR - Roles of extracellular matrix in neural development. Ann Rev Physiol 45: 581, 1983.
15. Yajima K, Suzuki K - Demyelination and remyelination in the rat central nervous system following ethidium bromide injection. Lab Invest 41: 385, 1979.

Datas de Publicação

Publicação nesta coleção
06 Jun 2011
Data do Fascículo
Set 1989

This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

[1] 1. Beck DW, Hart MN, Cancilla PA - The role of the macrophage in microvascular regeneration following brain injury. J Neuropath Exp Neurol 42: 601, 1983.

[2] 2. Blakemore WF - Remyelination by Schwann cells of axons demyelinated by intraspinal injection of 6-aminonicotinamide in the rat. J Neurocyt 4: 745, 1975.

[3] 3. Blakemore WF - Invasion of Schwann cells into the spinal cord of the rat following local injections of lysolecithin. Neuropath Appl Neurobiol 2: 21, 1976.

[4] 4. Blakemore WF - Ethidium bromide induced demyelination in the spinal cord of the cat. Neuropath Appl Neurobiol 8: 365, 1982.

[5] 5. Blakemore WF, Crang AJ - The use of cultured autologous Schwann cells to remyelinate areas of persistent demyelination in the central nervous system. J Neurol Sci 70: 207. 1985.

[6] 6. Blakemore WF, Eames RA, Smith KJ, McDonald WI - Remyelimation in the spinal cord of the cat following intraspinal injections of lysolecithin. J Neurol Sci 33: 31, 1977.

[7] 7. Blakemore WF, Patterson RC - Suppression of remyelination in the CNS by X-irradiation. Acta Neuropath (Berlin) 42: 105, 1978.

[8] 8. Bunge RP, Bunge MB - Evidence that contact with connective tissue matrix is required for normal interaction between Schwann cells and nerve fibres. J Cell Biol 78: 943, 1978.

[9] 9. Bunge RP, Bunge MB, Cochran M - Some factors influencing the proliferation and differentiation of myelin-forming cells. Neurology 28:59, 1978.

[10] 10. Folkman J - Angiogenesis: initiation and control. Ann NY Acad Sci 401: 212, 1982.

[11] 11. Graça DL - Investigation into ethidium bromide induced demyelination in the central nervous system. PhD Thesis, University of Cambridge, UK. Cambridge, 1986.

[12] 12. Graça DL, Blakemore WF - Delayed remyelination in rat spinal cord following ethidium bromide injection. Neuropath Appl Neurobiol 12: 593, 1986.

[13] 13. Polverini PJ, Cotran RS, Gimbrone MA Jr, Unanue ER - Activated macrophages induce vascular proliferation. Nature 269: 804, 1977.

[14] 14. Sanes JR - Roles of extracellular matrix in neural development. Ann Rev Physiol 45: 581, 1983.

[15] 15. Yajima K, Suzuki K - Demyelination and remyelination in the rat central nervous system following ethidium bromide injection. Lab Invest 41: 385, 1979.