Avaliação da atividade locomotora após indução local de desmielinização tóxica no tronco encefálico de ratos Wistar

Abstract

RESUMO -Lesões desmielinizantes induzidas pelo gliotóxico brometo de etídio (BE) têm sido estudadas com o objetivo de permitir a compreensão do limitado processo de re p a ro mielínico no sistema nerv o s o central, bem como avaliar estratégias terapêuticas no sentido de acelerar a re c o n s t rução das bainhas de mielina perdidas. Muito embora estudos eletrofisiológicos correlacionando situações de desmielinização e remielinização experimental sejam bem estabelecidos, os efeitos comportamentais não têm sido adequadamente investigados. Neste estudo, foram analisadas ultra-estruturalmente as lesões desmielinizantes e a atividade locomotora de ratos submetidos à indução focal de desmielinização pelo modelo do BE na s u p e rfície ventral do tronco encefálico, mediante observação de sua movimentação e controle motor durante a travessia de uma trave elevada de madeira (beam walking test). Foi observada a ocorrência de deficiências locomotoras até 31 dias pós-injeção de BE, constatando-se ainda que a subseqüente remielinização estava relacionada com o retorno da função perdida.PALAVRAS-CHAVE: brometo de etídio, desmielinização, ratos, remielinização, teste da passarela elevada. Evaluation of locomotor activity after a local induction of toxic demyelination in the brainstem of Wistar ratsABSTRACT -Ethidium-bromide (EB) -induced lesions have been used to investigate the incomplete re m y elination in the central nervous system, as well as to evaluate therapeutic strategies to accelerate the re c o n s t ruction of the lost myelin sheaths. Although many electrophysiologic studies were perf o rmed in situations of experimental demyelination and remyelination, their behavioural effects have not been pro p e r l y analyzed. In this study, we investigated ultrastructurally the EB -demyelinating lesions as well as the locomotor activity of rats during the beam walking test after a focal induction of demyelination using the EB model in the ventral surface of the brainstem. It was observed the occurrence of locomotor deficits until 31 days post-injection, as well as that subsequent remyelination was related to the re t u rn of the lost function.KEY WORDS: beam walking test, demyelination, ethidium bromide, rats, remyelination. infiltrantes e de células de Schwann, as últimas acabando por contribuir para o re p a ro mielínico central 8,10 . A remielinização das lesões desmielinizantes tem sido obtida com sucesso através da transplantação de células gliais 1 5 , 1 6 , sugerindo a possibilidade de re p a ro das lesões observadas em doenças como a e s c l e rose múltipla dos seres humanos e a cinomose dos cães com o uso de enxertos de células mielinogê-nicas. No entanto, antes que sua aplicação clínica possa ser contemplada, as conseqüências funcionais da desmielinização e da remielinização espontânea Diversos estudos acerca da desmielinização e da remielinização no sistema nervos central (SNC) têm sido empreendidos baseados no emprego do brometo de etídio (BE), uma droga intercalante gliotóxi-c a 1 -1 4 . Neste modelo, observa-s...

The Impact of Purinergic System Enzymes on Noncommunicable, Neurological, and Degenerative Diseases

“…Since the beginning of demyelination processes, the appearance of multiple plates in the white matter of brain and spinal cord can occur [ 179 ]. These lesions lead to the disability or complete loss of nerve impulses that result in the appearance of clinical manifestations such as motor impairment [ 180 ], blurred vision, hyperalgesia in the upper and lower limbs, excessive tiredness, weakness, anxiety, depression, and irreversible neurological deficits [ 179 , 181 , 182 ]. The remission is a subsequent phase characterized by the remyelination and tissue repair, with partial or complete disappearance of symptoms [ 176 ].…”

Effects of aquatic exercises in a rat model of brainstem demyelination with ethidium bromide on the beam walking test

“…It is characterized as an auto-immune disease that causes destruction of oligodendrocytes and, consequently, loss of the myelin sheath. This myelin loss causes a great variability of pathologic conditions [2][3][4] . Although its etiology is unknown 5 , it is postulated that genetic and environmental factors causes self-destructive lesions in the central nervous system, specifically against the white matter [5][6][7] .…”

“…The demyelinated animals made fewer steps than the non-demyelinated ones. some studies report that the animals receiving eB injection develop motor deficits until day 31, but not anymore on day 35 after lesion 4,17 . The presence of these deficits may contribute to the decrease in the number of footsteps taken by the demyelinated animals, probably due to motor limitation during locomotion and uncertainty to perform the steps needed to complete the elevated beam traverse.…”

“…The presence of these deficits may contribute to the decrease in the number of footsteps taken by the demyelinated animals, probably due to motor limitation during locomotion and uncertainty to perform the steps needed to complete the elevated beam traverse. one study correlated the motor inaptitude to oligodendrocyte loss and, consequently, to the demyelination caused by the action of eB 4 . The main point, however, was a reduction in the number of steps across days in group 1 like the non-demyelinated animals, suggesting a better motor performance in the group with aquatic exercises practice.…”

“…such process might have happened with our animals. The animals studied were young, which may contribute to a greater difficulty in performing the tasks, since most studies using the experimental model of eB used 3-4 monthold animals at the start of the experiments 3,4 .…”