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Neuroscience. 1999;92(3):827-39.

Primary cortical glial reaction versus secondary thalamic glial response in the excitotoxically injured young brain: astroglial response and metallothionein expression.

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Department of Cell Biology and Physiology, Autonomous University of Barcelona, Bellaterra, Spain.


In this study we have evaluated the primary astroglial reactivity to an injection of N-methyl-D-aspartate into the right sensorimotor cortex, as well as the secondary astroglial response in the thalamic ventrobasal complex, caused by the anterograde degeneration of descending corticothalamic fibres and/or target deprivation of the developing thalamic neurons. The astroglial response was evaluated from 4 h to 30 days post-lesion, by the immunocytochemical detection of the cytoskeletal proteins glial fibrillary acidic protein and vimentin, and the antioxidant and metal binding protein metallothionein I-II. In the lesioned cortex, hypertrophied reactive astrocytes showed increased glial fibrillary acidic protein labelling that correlated with a strong expression of vimentin and metallothionein I-II. Maximal astrocytic response was seen at one week post-lesion. The glial scar that formed later on remained positive for all astroglial markers until the last survival time examined. In contrast, in the anterogradely/retrogradely affected thalamus, the induced astroglial secondary response was not as prominent as in the cortex and was characteristically transitory, being undetectable by 14 days post-lesion. Interestingly, thalamic reactive astrocytes showed increased glial fibrillary acidic protein expression but no induction of vimentin and metallothionein I-II. In conclusion, in the young brain, the pattern of astroglial reactivity is not homogeneous and is strongly dependent on the grade of tissue damage: both in response to primary neuronal death and in response to retrograde/anterograde secondary damage, reactive astrocytes show hypertrophy and increased glial fibrillary acidic protein expression. However, astroglial vimentin and metallothionein I-II expression are only observed in areas undergoing massive neuronal death, where glial scar is formed.

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