title: Primary cortical glial reaction versus secondary thalamic glial response in the excitotoxically injured young brain: astroglial response and metallothionein expression.
abstract: 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.
authors.affiliation: Department of Cell Biology and Physiology, Autonomous University of Barcelona, Bellaterra, Spain.
authors.forename: L
authors.initials: L
authors.lastname: Acarin
authors.forename: B
authors.initials: B
authors.lastname: González
authors.forename: J
authors.initials: J
authors.lastname: Hidalgo
authors.forename: A J
authors.initials: AJ
authors.lastname: Castro
authors.forename: B
authors.initials: B
authors.lastname: Castellano
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000187:drug effects / Q000473:pathology / Q000502:physiology*; D001921:Brain / Q000187:drug effects* / Q000473:pathology / Q000503:physiopathology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology*; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D007267:Injections; D008668:Metallothionein / Q000378:metabolism; D016202:N-Methylaspartate / Q000494:pharmacology*; D009498:Neurotoxins / Q000494:pharmacology*; D051381:Rats; D020318:Rats, Long-Evans; D013003:Somatosensory Cortex / Q000187:drug effects* / Q000473:pathology / Q000503:physiopathology*; D013788:Thalamus / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology*; D014746:Vimentin / Q000378:metabolism
chemical_list: D018691:Excitatory Amino Acid Antagonists; D005904:Glial Fibrillary Acidic Protein; D009498:Neurotoxins; D014746:Vimentin; D016202:N-Methylaspartate; D008668:Metallothionein