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

• Published in: Neuroscience 1999-01, Vol.92 (3), p.827-839
• Main Authors: Acarin, L., González, B., Hidalgo, J., Castro, A.J., Castellano, B.
• Format: Article
• Language: English
• Subjects: Animals; Astrocytes - drug effects; Astrocytes - pathology; Astrocytes - physiology; Biological and medical sciences; Brain - drug effects; Brain - pathology; Brain - physiopathology; development; Development. Senescence. Regeneration. Transplantation; Excitatory Amino Acid Antagonists - pharmacology; Fundamental and applied biological sciences. Psychology; Glial Fibrillary Acidic Protein - metabolism; Injections; Metallothionein - metabolism; N-Methylaspartate - pharmacology; Neurotoxins - pharmacology; postnatal; rat; Rats; Rats, Long-Evans; retrograde changes; Somatosensory Cortex - drug effects; Somatosensory Cortex - pathology; Somatosensory Cortex - physiopathology; Thalamus - drug effects; Thalamus - pathology; Thalamus - physiopathology; VB complex; Vertebrates: nervous system and sense organs; vimentin; Vimentin - metabolism
• ISSN: 0306-4522; 1873-7544
• DOI: 10.1016/S0306-4522(99)00022-6

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.