Schwann cell expression of an oligodendrocyte-like remyelinating pattern after ethidium bromide injection in the rat spinal cord / Expressão pelas células de Schwann de um padrão de remielinização semelhante ao oligodendroglial após injeção de brometo de etídio na medula espinhal de ratos

Schwann cells are recognized by their capacity of producing single internodes of myelin around axons of the peripheral nervous system. In the ethidium bromide (EB) model of primary demyelination in the brainstem, it is observed the entry of Schwann cells into the central nervous system in order to contribute to the myelin repair performed by the oligodendrocytes that survived to the EB gliotoxic action, being able to even remyelinate more than one axon at the same time, in a pattern of repair similar to the oligodendroglial one. The present study was developed in the spinal cord to observe if Schwann cells maintained this competence of attending simultaneously different internodes. It was noted that, on the contrary of the brainstem, Schwann cells were the most important myelinogenic cells in the demyelinated site and, although rare, also presented the capacity of producing more than one internode of myelin in distinct axons.

As células de Schwann são reconhecidas por sua capacidade de produzir internodos de mielina únicos ao redor de axônios do sistema nervoso periférico. No modelo de desmielinização primária do brometo de etídio (BE) no tronco encefálico, tem sido observada a entrada destas células no sistema nervoso central. Isso pode contribuir para o reparo mielínico desempenhado pelos oligodendrócitos que sobreviveram à ação glitóxica do BE, chegando a remielinizar mais de um axônio ao mesmo tempo, em um padrão de reparo semelhante ao oligodendroglial. O presente estudo foi realizado na medula espinhal para observar se as células de Schwann mantinham esta competência de atender simultaneamente diferentes internodos. Foi observado que, ao contrário do tronco encefálico, as células de Schwann foram as células mielinogênicas mais importantes no sítio de desmielinização induzida pelo BE e, embora raro, também apresentaram a capacidade de produzir mais de um internodo de mielina em axônios distintos.

OSP-Immunofluorescent remyelinating oligodendrocytes in the brainstem of toxically-demyelinated Wistar rats

A remielinização do sistema nervoso central após desmielinização tóxica é um processo bem conhecido. No encéfalo, os oligodendrócitos remielinizam uma área maior do que na medula espinhal, onde as células de Schwann são preponderantes. Embora esses fatos sejam bem conhecidos, ainda não se conhece com certeza a origem das células remielinizantes. Esta investigação foi desenhada para esclarecer a participação de oligodendrócitos maduros na reconstrução das bainhas perdidas após a desmielinização induzida por brometo de etídio (BE) no tronco encefálico de ratos Wistar normais e imunossuprimidos com ciclosporina A. Trinta ratos fêmeas adultas foram divididos em três grupos experimentais. No grupo 1, os ratos receberam uma injeção de 10 mL de BE em 0,9% salina (n=10) na cisterna basal; no grupo 2, os ratos receberam a injeção de BE e foram tratados com ciclosporina A (n=10); no grupo 3 os ratos receberam uma injeção de 10 mL de 0,9% salina e foram tratados com ciclosporina A. Os ratos foram sacrificados aos 15, 21 e 31 dias após a injeção. A partir dos 15 dias muitas células da periferia das lesões tiveram marcação positiva para OSP (proteína específica do oligodendrócito), marcador de oligodendrócitos maduros e mielina. Assim, foi possível comprovar que células maduras da linhagem oligodendroglial participam do processo de remielinização neste modelo gliotóxico.

Delayed Schwann cell and oligodendrocyte remyelination after ethidium bromide injection in the brainstem of Wistar rats submitted to streptozotocin diabetogenic treatment

Schwann cell disturbance followed by segmental demyelination in the peripheral nervous system occurs in diabetic patients. Since Schwann cell and oligodendrocyte remyelination in the central nervous system is a well-known event in the ethidium bromide (EB) demyelinating model, the aim of this investigation was to determine the behavior of both cell types after local EB injection into the brainstem of streptozotocin diabetic rats. Adult male Wistar rats received a single intravenous injection of streptozotocin (50 mg/kg) and were submitted 10 days later to a single injection of 10 æL 0.1 percent (w/v) EB or 0.9 percent saline solution into the cisterna pontis. Ten microliters of 0.1 percent EB was also injected into non-diabetic rats. The animals were anesthetized and perfused through the heart 7 to 31 days after EB or saline injection and brainstem sections were collected and processed for light and transmission electron microscopy. The final balance of myelin repair in diabetic and non-diabetic rats at 31 days was compared using a semi-quantitative method. Diabetic rats presented delayed macrophage activity and lesser remyelination compared to non-diabetic rats. Although oligodendrocytes were the major remyelinating cells in the brainstem, Schwann cells invaded EB-induced lesions, first appearing at 11 days in non-diabetic rats and by 15 days in diabetic rats. Results indicate that short-term streptozotocin-induced diabetes hindered both oligodendrocyte and Schwann cell remyelination (mean remyelination scores of 2.57 ± 0.77 for oligodendrocytes and 0.67 ± 0.5 for Schwann cells) compared to non-diabetic rats (3.27 ± 0.85 and 1.38 ± 0.81, respectively).

Behaviour of oligodendrocytes and Schwann cells in an experimental model of toxic demyelination of the central nervous system

Oligodendrocytes and Schwann cells are engaged in myelin production, maintenance and repairing respectively in the central nervous system (CNS) and the peripheral nervous system (PNS). Whereas oligodendrocytes act only within the CNS, Schwann cells are able to invade the CNS in order to make new myelin sheaths around demyelinated axons. Both cells have some limitations in their activities, i.e. oligodendrocytes are post-mitotic cells and Schwann cells only get into the CNS in the absence of astrocytes. Ethidium bromide (EB) is a gliotoxic chemical that when injected locally within the CNS, induce demyelination. In the EB model of demyelination, glial cells are destroyed early after intoxication and Schwann cells are free to approach the naked central axons. In normal Wistar rats, regeneration of lost myelin sheaths can be achieved as early as thirteen days after intoxication; in Wistar rats immunosuppressed with cyclophosphamide the process is delayed and in rats administered cyclosporine it may be accelerated. Aiming the enlightening of those complex processes, all events concerning the myelinating cells in an experimental model are herein presented and discussed

Cross-talk between neurons and glia: highlights on soluble factors

The development of the nervous system is guided by a balanced action between intrinsic factors represented by the genetic program and epigenetic factors characterized by cell-cell interactions which neural cells might perform throughout nervous system morphogenesis. Highly relevant among them are neuron-glia interactions. Several soluble factors secreted by either glial or neuronal cells have been implicated in the mutual influence these cells exert on each other. In this review, we will focus our attention on recent advances in the understanding of the role of glial and neuronal trophic factors in nervous system development. We will argue that the functional architecture of the brain depends on an intimate neuron-glia partnership

O papel das celulas satelites nas respostas adaptativas do tecido muscular esqueletico / The role of satellite cells on adaptatives states of skeletal muscle tissue

O tecido muscular esqueletico e sensivel a modificacoes agudas e cronicas induzidas por exercicios. As celulas satelites (CS) estao diferentemente envolvidas nas respostas de carater regenerador e nos processos de hipertrofia e hiperplasia no musculo adulto...

Proliferation of differentiated glial cells in the brain stem

Classical studies of macroglial proliferation in muride rodents have provided conflicting evidence concerning the proliferating capabilities of oligodendrocytes and microglia. Furthermore, little information has been obtained in other mammalian orders and very little is known about glial cell proliferation and differentiation in the subclass Metatheria although valuable knowledge may be obtained from the protracted period of central nervous system maturation in these forms. Thus, we have studied the proliferative capacity of phenotypically identified brain stem oligodendrocytes by tritiated thymidine radioautography and have compared it with known features of oligodentroglial differentation as well as with proliferation of microglia in the opossum Didelphis marsupialis. We have detected a previously undescribed ephemeral, regionally heterogenous proliferation of oligodendrocytes expressing the actin-binding, ensheathment-related protein 2' 3'- cyclic nucleotide 3' -phosphodiesterase (CNPase), that is not necessarily related to the known regional and temporal heterogeneity of expression of CNPase in cell bodies. On the other hand, proliferation of microglia tagged by the binding of Griffonia simplicifolia B4 isolectin, which recognizes an alpha-D-galactosyl-bearing glycoprotein of the plasma membrane of macrophages/microglia, is known to be long lasting, showing no regional heterogeneity and being found amongst both ameboid and differentiated ramified cells, although at different rates. The functional significance of the proliferative behavior of these differentiated cells is unknown but may provide a lowgrade cell renewal in the normal brain and may be augmented under pathological conditions.

Biology of the repair of central nervous system demyelinated lesions

The integrity of myelin sheaths is maintained by oligodendrocytes and Schwann cells respectively in the central nervous system (CNS) and in the peripheral nervous system. The process of demyelination consistin of the withdrawal of myelin sheaths from their axons is a characteristic feature of multiple sclerosis, the most common human demyelinating disease. Many experimental models have been designed to study the biology of demyelination and remyelination (repair of the lost myelin) in the CNS, due to the difficulties in studying human material. In the ethidium bromide (an intercalating gliotoxic drug) model of demyelination, CNS remyelination may be carried out by surviving oligodendrocytes and/or by cells differentiated from the primitive cell lines or either by Schwann cells that invade the CNS. However, some factor such as the age of the experimental anmnals, intensity and time of exposure to the intercalating clinical and the topography of the lesions have marked influente on the repair of the tissue.

Mielinizaçäo, desmielinizaçäo e remielinizaçäo no sistema nervoso central / Myelination, demyelination and remyelination in the central nervous system

As bainhas de mielina que envolvem axônios no SNC säo feitas e mantidas por oligodendrócitos. Esta células gliais formam um número variável de segmentos de mielina (internódulos): entre 1 e 200, de modo que quando uma célula é lesada junto com ela podem ser destruídos numerosos internódulos, constituindo um processo desmielinizante. Como conseqüência da destruiçäo da célula-bainha e internódulos relacionados há uma resposta celular rápida e abundante. Esta resposta é feita por fagócitos residentes (microglia) e hematógenos. Ambas as células fagocitam os detritos celulares e de mielina, deixando os axônios desmielinizados. Estes axônios podem permanecer desprovidos de suas bainhas e aglutinados, podem ser separados por processos de astrócitos ou podem ser remielinizados. A ocorrência do processo de remielinizaçäo depende da intensidade e tempo de exposiçäo ao agente desmielinizante. A remielinizaçäo, com total restabelecimento da conduçäo pode ser realizada por oligodendrócito ou por célula de Schwann que invade o SNC sempre que os astrócitos säo destruídos