RESUMEN
Spinal cord injury (SCI), which is much in the public eye, is still a refractory disease compromising the well-being of both patients and society. In spite of there being many methods dealing with the lesion, there is still a deficiency in comprehensive strategies covering all facets of this damage. Further, we should also mention the structure called the corticospinal tract (CST) which plays a crucial role in the motor responses of organisms, and it will be the focal point of our attention. In this review, we discuss a variety of strategies targeting different dimensions following SCI and some treatments that are especially efficacious to the CST are emphasized. Over recent decades, researchers have developed many effective tactics involving five approaches: (1) tackle more extensive regions; (2) provide a regenerative microenvironment; (3) provide a glial microenvironment; (4) transplantation; and (5) other auxiliary methods, for instance, rehabilitation training and electrical stimulation. We review the basic knowledge on this disease and correlative treatments. In addition, some well-formulated perspectives and hypotheses have been delineated. We emphasize that such a multifaceted problem needs combinatorial approaches, and we analyze some discrepancies in past studies. Finally, for the future, we present numerous brand-new latent tactics which have great promise for curbing SCI.
Asunto(s)
Animales , Humanos , Astrocitos/citología , Axones/fisiología , Trasplante de Células , Modelos Animales de Enfermedad , Estimulación Eléctrica , Microglía/citología , Neuronas Motoras/citología , Regeneración Nerviosa , Neuroglía/citología , Plasticidad Neuronal , Neuronas/citología , Oligodendroglía/citología , Tractos Piramidales/patología , Recuperación de la Función , Medicina Regenerativa/métodos , Traumatismos de la Médula Espinal/terapiaRESUMEN
Endothelin (ET)-1 and its receptors (ETA and ETB receptor) are present in the central nervous system. ET exerts biological effects on gliogenesis and glial cell functions. In order to define a possible mechanism of ETA receptor signaling, the distribution of the ETA receptor in developing oligodendrocytes and the effects of ET-1 on the myelination of oligodendrocytes were examined. ETA receptor immunoreactivity was confined to the perivascular elements of the blood vessels during early postnatal development. However later in development, ETA receptor immunoreactivity was no longer observed in the vessels but became localized to the myelinating oligodendrocytes of the primitive corpus callosum of the white matter, apart from the vessels. ET-1 induced myelin basic protein (MBP) in primary oligodendrocyte precursor cell culture though the ETA receptor and was blocked by an ETA receptor antagonist. In addition, ET-1 evoked the release of Ca2+ which is a central regulator of oligodendrocyte differentiation. Our results provide a link between ET-1 and its ETA receptor and myelination during oligodendrocyte differentiation.
Asunto(s)
Animales , Ratones , Ratas , Encéfalo/patología , Calcio/metabolismo , Señalización del Calcio , Células Cultivadas , Endotelina-1/metabolismo , Ratones Endogámicos ICR , Proteína Básica de Mielina/genética , Vaina de Mielina/fisiología , Oligodendroglía/citología , Ratas Sprague-Dawley , Receptor de Endotelina A/metabolismoRESUMEN
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.