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Characteristics of Glial Reaction in the Perinatal Rat Cortex: Effect of Lesion Size in the ‘Critical Period’

Mihály Kálmán, Béla M. Ajtai, Jon Håvard Sommernes

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Abstract

In this study we investigate the capability of lesions, performed between embryonic day E18 and postnatal day P6, to provoke glial reaction. Two different lesion types were applied: 'severe' lesion (tissue defect) and 'light' lesion (stab wound). The glial reaction was detected with immunostaining against glial fibrillary acidic protein. When performed as early as P0, severe lesions could result in reactive gliosis, which persisted even after a month. The glial reaction was detected at P6/P7 and became strong by P8, regardless of the age when the animals were lesioned between P0 and P5. Namely, a strict limit could be estimated for the age when reactive glia were already found rather than for the age when glial reaction-provoking lesions could occur. After prenatal lesions, no glial reaction developed, but the usual glia limitans covered the deformed brain surface. Light lesions provoked glial reactions when performed at P6. In conclusion, three scenarios were found, depending on the age of the animal at injury: (i) healing without glial reaction, regardless of the remaining deformation; (ii) depending on the size of the lesion, either healing without residuum or with remaining tissue defect plus reactive gliosis; and (iii) healing always with reactive gliosis. The age limits between them were at P0 and P5. The glial reactivity seemingly appears after the end of the neuronal migration and just precedes the massive transformation of the radial glia into astrocytes. Estimating the position of the appearance of glial reactivity among the events of cortical maturation can help to adapt the experimental results to humans.

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What this paper is about

In this study we investigate the capability of lesions, performed between embryonic day E18 and postnatal day P6, to provoke glial reaction. Two different lesion types were applied: 'severe' lesion (tissue defect) and 'light' lesion (stab wound). The glial reaction was detected with immunostaining against glial fibrillary acidic protein. When performed as early as P0, severe lesions could result in reactive gliosis, which persisted even after a month. The glial reaction was detected at P6/P7 and became strong by P8, regardless of the age when the animals were lesioned between P0 and P5. Namely, a strict limit could be estimated for the age when reactive glia were already found rather than for the age when glial reaction-provoking lesions could occur. After prenatal lesions, no glial reaction developed, but the usual glia limitans covered the deformed brain surface. Light lesions provoked glial reactions when performed at P6. In conclusion, three scenarios were found, depending on the age of the animal at injury: (i) healing without glial reaction, regardless of the remaining deformation; (ii) depending on the size of the lesion, either healing without residuum or with remaining tissue defect plus reactive gliosis; and (iii) healing always with reactive gliosis. The age limits between them were at P0 and P5. The glial reactivity seemingly appears after the end of the neuronal migration and just precedes the massive transformation of the radial glia into astrocytes. Estimating the position of the appearance of glial reactivity among the events of cortical maturation can help to adapt the experimental results to humans.

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Available abstract

In this study we investigate the capability of lesions, performed between embryonic day E18 and postnatal day P6, to provoke glial reaction. Two different lesion types were applied: 'severe' lesion (tissue defect) and 'light' lesion (stab wound). The glial reaction was detected with immunostaining against glial fibrillary acidic protein. When performed as early as P0, severe lesions could result in reactive gliosis, which persisted even after a month. The glial reaction was detected at P6/P7 and became strong by P8, regardless of the age when the animals were lesioned between P0 and P5. Namely, a strict limit could be estimated for the age when reactive glia were already found rather than for the age when glial reaction-provoking lesions could occur. After prenatal lesions, no glial reaction developed, but the usual glia limitans covered the deformed brain surface. Light lesions provoked glial reactions when performed at P6. In conclusion, three scenarios were found, depending on the age of the animal at injury: (i) healing without glial reaction, regardless of the remaining deformation; (ii) depending on the size of the lesion, either healing without residuum or with remaining tissue defect plus reactive gliosis; and (iii) healing always with reactive gliosis. The age limits between them were at P0 and P5. The glial reactivity seemingly appears after the end of the neuronal migration and just precedes the massive transformation of the radial glia into astrocytes. Estimating the position of the appearance of glial reactivity among the events of cortical maturation can help to adapt the experimental results to humans.

Key concepts: Period (music), Lesion, Cortex (anatomy), Neuroscience, Cerebral cortex, Perinatal period, Medicine, Biology

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Characteristics of Glial Reaction in the Perinatal Rat Cortex: Effect of Lesion Size in the ‘Critical Period’ — Research Paper | ScholarLens