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

In this study we have evaluated the primary astroglial reactivity to an inj ection of N-methyl-D-aspartate into the right sensorimotor cortex, as well as the secondary astroglial response in the thalamic ventrobasal complex, c aused by the anterograde degeneration of descending corticothalamic fibres and/or target deprivation of the developing thalamic neurons. The astroglia l response was evaluated from 4 h to 30 days post-lesion, by the immunocyto chemical detection of the cytoskeletal proteins glial fibrillary acidic pro tein and vimentin, and the antioxidant and metal binding protein metallothi onein I-II. In the lesioned cortex, hypertrophied reactive astrocytes showe d increased glial fibrillary acidic protein labelling that correlated with a strong expression of vimentin and metallothionein I-II. Maximal astrocyti c response was seen at one week post-lesion. The glial scar that formed lat er on remained positive for all astroglial markers until the last survival time examined. In contrast, in the anterogradely/retrogradely affected thal amus, 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 increa sed 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: ba th in response to primary neuronal death and in response to retrograde/ante rograde secondary damage, reactive astrocytes show hypertrophy and increase d glial fibrillary acidic protein expression. However, astroglial vimentin and metallothionein I-II expression are only observed in areas undergoing m assive neuronal death, where glial scar is formed. (C) 1999 IBRO. Published by Elsevier Science Ltd.